scholarly journals A Case of Mistaken Identity: TTP-like State Due to Heroin Overdose

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4905-4905
Author(s):  
Phani Borra ◽  
Cory Edward Mellon
Keyword(s):  
Plasma Exchange ◽  
Clinical Picture ◽  
Total Bilirubin ◽  
Conflicts Of Interest ◽  
Adverse Outcomes ◽  
Learning Objective ◽  
Severe Thrombocytopenia ◽  
Alcoholic Fatty Liver ◽  
Increased Risk ◽  
Ct Head

Learning Objective 1: Recognize that multiple etiologies can play a role in the overall presentation of patient's thrombocytopenia. Learning Objective 2: Rethink the original working diagnosis when there is discordance with clinical picture. Case: 52-year old male with a PMHx of heroin and alcohol abuse presented to ED after being found unresponsive due to heroin OD. Patient (Pt) was initially seen in the ED 4days prior for left leg cellulitis and was sent home on oral Bactrim. Lab values during that visit showed a platelet (plt) count of 80 K/UL, Hgb 10.1 g/dl and creatinine (Cr) of 1.46 mg/dl. On his 2nd ED visit, his WBC count was 12.7 K/UL, Hgb 7.7g/dl, plt 23K/UL, haptoglobin <8.0mg/dl and reticulocyte count of 4.1%. His BUN and Cr were elevated at 32 mg/dl and 2.97mg/dl respectively and UA showed large blood with 3-5 RBC, CPK was 24806 IU/L, LFTs demonstrated an AST of 414 IU/L, ALT of 90 IU/L, total bilirubin 2.0mg/dl, direct bilirubin 0.8mg/dl, LDH of 2339 IU/L and ESR >140 mm/hr. Coagulation parameters were normal. Pt's urine toxicology was positive for opiates and methadone. Manual differential was initially negative for schistocytes, helmet cells or bite cells. HIV was non-reactive, RPR and acute hepatitis panel were negative. On exam, pt was drowsy, had icteric sclera and faint left pedal pulses without purpuric rash. Pt was started on IV fluids for oliguric AKI and rhabdomyolysis. Arterial doppler revealed no detectable blood flow in his left distal superficial femoral, tibial and popliteal arteries. Initial CT head was negative for acute findings. Hematology consulted for possible diagnosis of TTP. Consultant didn't think clinical picture was consistent with TTP as total bilirubin at the time of consultation was normal therefore plasma exchange wasn't recommended. However, primary service still considered TTP highest on the differential therefore, ADAMTS13 was ordered but no plasma exchange was initiated. Given the fact pt received oral Bactrim for diagnosis of lower extremity cellulitis, G6PD deficiency was included in the differential however, testing was done early after hemolytic event and while reticulocytes were elevated, therefore results were not diagnostic. Of note, plts were transfused per vascular surgery prior to a planned thrombectomy of left leg, and plts increased to 81 K/UL. Pt underwent unsuccessful left leg thrombectomy due to chronic changes in the vessels and collaterals. CPK levels continued to increase and renal function continued to worsen as did his mental status. Pt was started on hemodialysis (HD) by end of 2nd day. There was persistent effort to incorporate all lab derangements into one all-inclusive diagnosis. Hematology was asked to review the case again as pt's plts continued to drop, ADAMTS13 activity was low at <2.0% and schistocytes were now noted on the peripheral smear. TTP was again not seen as the primary cause of the pt's clinical picture as total bilirubin continued to be normal, schistocytes only appeared after HD was initiated and low ADAMTS13 was thought to be secondary to liver dysfunction, inflammation and heroin OD. A repeat CT-head done showed left cerebellar hypodensities suspicious for acute CVA. Pt continued to deteriorate requiring mechanical ventilation. Troponins were checked which showed a level of 31.90ng/dl and ECG done simultaneously showed sinus tachycardia and no ischemic changes. Cardiology was consulted who determined trop elevation was likely due to skeletal muscle injury and possibly due to NSTEMI. However, due to pt's severe thrombocytopenia, Cardiology determined he was not a candidate for antiplatelet therapy or anticoagulation. Despite aggressive resuscitative measures, patient died Discussion: We reviewed the literature to evaluate other causes of this pt's clinical picture. While pt has overlapping features of TTP except fever, other causes for his mild hemolytic anemia and low plts include polysubstance abuse, rhabdomyolysis, poor nutritional status, presence of alcoholic fatty liver and uremia. Thrombocytopenia is associated with an increased risk of adverse outcomes, regardless of the causes. It has been documented in literature that heroin OD can cause rhabdomyolysis, renal failure, cardiac dysfunction, and permanent neurologic complications. The original diagnosis of TTP was anchored on and we persisted in trying to make the clinical picture fit that diagnosis and delayed in looking at overall clinical picture of the pt. Disclosures No relevant conflicts of interest to declare.

Thienopyridine-Associated Thrombotic Thrombocytopenia Purpura: Updated Antibody Results From the SERF-TTP Study.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 892-892
Author(s):  
Anaadriana Zakarija ◽  
Thanh Ha Luu ◽  
Hau C. Kwaan ◽  
June McKoy ◽  
Ivy Weiss ◽  
...  
Keyword(s):  
Plasma Exchange ◽  
Neutralizing Antibodies ◽  
Conflicts Of Interest ◽  
Therapeutic Plasma Exchange ◽  
Severe Thrombocytopenia ◽  
Adamts13 Activity ◽  
Laboratory Findings ◽  
History Of ◽  
Adamts13 Deficiency ◽  
Drug Dependent

Abstract Abstract 892 Background: The thienopyridines, ticlopidine and clopidogrel, have been associated with thrombotic thrombocytopenia purpura (TTP). However, few studies have reported information on antibodies to ADAMTS13 among patients with thienopyridine-associated TTP. We previously reported on two mechanistic pathways of thienopyridine-associated TTP with some overlapping features. Evaluation of ADAMTS13 autoantibodies was undertaken to improve understanding of these syndromes. Methods: Clinical and laboratory findings were evaluated for 30 ticlopidine-, 10 clopidogrel-associated TTP cases, and 54 cases of idiopathic TTP. Results: Among patients with thienopyridine-induced TTP, those with a history of ticlopidine versus clopidogrel use were more likely to present with severe thrombocytopenia (platelet < 20,000) (90% versus 13%), severe ADAMTS13-deficiency (80% versus 0%), and neutralizing antibodies to ADAMTS13 (100% versus 0%), and were less likely to have less than a two week history of thienopyridine exposure (0% versus 50%) (p<0.05 for each comparison). They were also more likely to survive following therapeutic plasma exchange (TPE) (85% versus 50%). 2 patients exposed to clopidogrel later relapsed and had similar characteristics to idiopathic TTP patients with non-deficient ADAMTS13 activity. Conclusion: Ticlopidine causes TTP by a pathway involving a neutralizing autoantibody to ADAMTS13 while clopidogrel causes TTP by an ADAMTS13-independent pathway. Although ADAMTS13 autoantibodies are present in both idiopathic and ticlopidine-associated TTP, spontaneous relapses are not seen in ticlopidine-associaated TTP, suggesting that drug-dependent antibodies are present. Clopidogrel associated TTP is distinct from idiopathic TTP in that ADAMTS13 autoantibodies are absent and response to TPE is poor. Disclosures: No relevant conflicts of interest to declare.

scholarly journals TLT-1, a Potential Regulator of Inflammatory Pathogenesis in Obesity and Non-Alcoholic Fatty Liver Disease (NAFLD)

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 1005-1005
Author(s):  
Siobhan Laken Branfield ◽  
Benjamin Nieves Lopez ◽  
Matthew E Poynter ◽  
Anthony Valance Washington
Keyword(s):  
Adipose Tissue ◽  
Histological Analysis ◽  
Conflicts Of Interest ◽  
Western Diet ◽  
Binding Motif ◽  
Pathophysiological Mechanism ◽  
Specific Receptor ◽  
Ligand Interaction ◽  
Alcoholic Fatty Liver ◽  
Increased Risk

Abstract Background: Obesity, a nationwide health issue, has related medical costs ranging between $147-210 billion per year in United States and has been associated with a 3.5-fold increased risk of developing NAFLD. In obesity, platelets work in a pleotropic manner with vascular and immune cells to amplify the chronic inflammatory process. Interestingly, studies have demonstrated that platelet numbers and reactivity are increased in obese individuals. The emerging role of activated platelets during obesity induced inflammation introduces the novel concept of platelet targeted therapeutic interventions. Kopec et al, further supports the idea that the mechanism underlying the progression of obesity lies in a platelet mediated pro-inflammatory state, illustrating that there is extravascular fibrin(ogen) deposition, macrophages and inflammatory cytokines within white adipose tissue and liver of mice on western diet. Kopec et al uses a fibrinogen mutant mouse (Fiby390-396 ) which lacks the binding motif for Mac-1 and inhibits the ligand interaction with leukocytes, diminishing inflammation, reducing macrophage counts, reducing weight, protects mice from NAFLD and glucose dysmetabolism. Taken together, all evidence points towards a platelet/fibrinogen/leukocyte pathophysiological mechanism underlying the development of obesity. TREM-Like Transcript-1 (TLT-1) is a platelet specific receptor found in the a-granules of platelets and released to the surface upon platelet activation. TLT-1 is a type 1 receptor that, like the integrin a2bb3, binds fibrinogen and facilitates platelet aggregation . However, although TLT-1 may assist in clot formation and hemostasis to arrest bleeding in a non-inflammatory/nonimmune mediated setting, TLT-1's main association is with regulating inflammatory-derived bleeding. This is demonstrated by increased hemorrhage after inflammatory treatments such as lipopolysaccharide LPS in the treml1 -/- mice as compared to controls. Considering the emerging evidence in support of a platelet-fibrinogen receptor ligand interaction as a key mechanism underlying the development of obesity and that TLT-1, a platelet specific receptor binds fibrinogen and mediates leukocyte trafficking, our laboratory set out to determine whether TLT-1 could be implicated as the main culprit underlying this mechanism. When placed on a western diet, treml1 -/-mice are more prone to weight gain, based on these finding we hypothesize that: The TLT-1/Fibrinogen molecular interaction regulates metabolic inflammation in obesity Aims: Evaluate the effects of western diet on obesity and NAFLD in the treml1 -/- mouse model Methods: TLT-1 (treml1 -/-) - apolipoprotein E (apoe -/-) double null (AT-DKO;n=11) mice and control apoe +/-/treml1 +/- littermate controls (AT-Hets;n=20) were fed western diet for 20 weeks. Plasma samples were collected for adipokine, glucose, insulin, liver enzyme and lipid profiling. Mouse were perfused, liver and adipose tissue were collected for histological analysis. Results: Overall AT-DKO mice gained more weight compared to AT-Hets (12.94±1.90 vs 8.51±1.70 grams p=0.02). Plasma analysis demonstrates that the AT-DKO have higher levels of TNF-a (0.54±0.60 vs 0.118±0.17 pg/ml p=0.03), and IL-10 (2.50±1.40 vs 1.50±2.10 pg/ml p=0.004) compared to littermate controls. Histological analysis of livers illustrates increased lipid vacuoles and inflammatory foci in the AT-DKO mice as compared to controls, while preliminary data is not significant for these differences, liver damage in the AT-DKO was significantly greater as demonstrated by increased AST levels (166.21±91.00 vs 102±68.10 U/L p=0.02). Moreover, the AT-DKO mice had higher levels of ALT, direct bilirubin, cholesterol, pai-1 , triglycerides and lower IL-6 and Adiponectin (Table 1 data not significant). These findings suggest that in the absence of TLT-1 these mice are more prone to liver disfunction , hyperlipidemia and inflammatory alterations. Conclusions: Mutant AT-DKO mice are more prone to obesity and NAFLD compared to littermate controls, suggesting that TLT-1, a platelet gene, plays a surprising role in metabolism. Further investigation could adjudicate TLT-1 administration as a potential therapeutic intervention for prevention and amelioration of Obesity and related pathologies. The current state of this project will be reported here. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

β2-Glycoprotein 1 Antibodies Directly Activate the Platelet IgG Receptor, FcγRIIa, and Cause Thrombosis in FCGR2A Transgenic but Not in Wild Type Mice

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 106-106
Author(s):  
Ali Amirkhosravi ◽  
Todd V Meyer ◽  
Liza Robles-Carrillo ◽  
Meghan Hatfield ◽  
Hina Desai ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Conflicts Of Interest ◽  
Degradation Products ◽  
Higher Order ◽  
Size Exclusion ◽  
Size Analysis ◽  
Severe Thrombocytopenia ◽  
Wild Type ◽  
Increased Risk ◽  
Induced Aggregation

Abstract Abstract 106 Antibodies targeting β2-glycoprotein 1 (β2-GP1; β2-Abs) are of primary importance in antiphospholipid syndrome (APS), a thrombotic autoimmune disorder. The predominance of the IgG antibody isotype in APS is conspicuously associated with increased risk of thrombosis, raising the question whether the platelet IgG receptor, FcγRIIa, may play a role in thrombosis in APS, as is the case in heparin-induced thrombocytopenia (HIT). The hypothesis that platelet FcγRIIa may contribute to thrombosis in APS has received little attention, with research emphasis instead placed on several proposed alternative mechanisms of action. We have shown that, like HIT antibodies, antibodies targeting VEGF or CD154 are also potently thrombotic in mice transgenic for human FcγRIIa but have no activity in mice lacking FcγRIIa (i.e., wild type mice). We therefore asked whether antiphospholipid antibodies can activate platelets and cause thrombosis via FcγRIIa. To this end, we tested mouse monoclonal (mAb) and goat polyclonal anti-human β2-Abs alone or complexed to human β2-glycoprotein 1 (i.e., to form immune complexes, or ICs) by the serotonin release assay (SRA) and platelet aggregation methods using washed human platelets. We found that two of three commercially available polyclonal anti-β2-Abs (pAb1 and pAb3), both alone or in IC form, induced platelet granule release and aggregation, and that this activity was abolished by anti-FcγRIIa mAb, IV.3. pAb2 and mAb were inactive. Activity analysis (SRA) of preformed ICs using constant pAb1 concentration with varied β2-GP1 stoichiometries revealed a zone-of-equivalence pattern, with maximal activity near balanced stoichiometry (1:1). Because pAb2 did not activate platelets, we sought to determine its capacity to form higher order ICs (which are known to be required for FcγRIIa activation) by size exclusion chromatography (SEC). All antibodies tested in isolation were shown by HPLC-SEC to be free of aggregates or degradation products. Antibody-antigen complex size analysis revealed that, as expected, mAb+β2-GP1 in 1:1 stoichiometry failed to form higher order ICs (i.e., complexes having ≥2 IgGs/complex). pAb2 (inactive) did form higher order ICs at 1:1 and 4:1 (IgG:Ag) stoichiometries, but less extensively than pAb1 (active), which efficiently formed higher order ICs at both 1:1 and 4:1 stoichiometries. pAb1 alone (i.e., not in IC form) caused aggregation, while pAb2 did not. Furthermore, preincubation of washed platelets with pAb2 prevented pAb1-induced aggregation, suggesting that pAb1 activity is β2-GP1-specific. A single intravenous injection of anti-β2-GP1 ICs (20 μg β2-GP1 plus 120 μg pAb1, a 1:2 molar stoichiometry) induced severe thrombocytopenia (>90%) and caused thrombotic shock in FcγRIIa-transgenic mice but not in wild type mice. Symptoms of shock occurred within 10 minutes. Pervasive occlusive thrombi were observed in the lungs of all FcγRIIa-transgenic but not in any wild type mice (H&E microscopy). Injection of pAb2 ICs produced none of these effects in transgenic or wild type mice. Finally, injection of pAb1 or pAb2 alone (neither of which bind mouse β2-GP1) had no effects in transgenic mice. In summary, these findings confirm previous in vitro studies that β2-Abs can directly activate platelets in a manner wholly dependent on the platelet IgG receptor, FcγRIIa. Additionally, we have shown for the first time in vivo that β2-Abs can also cause FcγRIIa-dependent thrombosis. This mechanism may contribute to thrombosis in APS, suggesting that further studies on the importance of FcγRIIa in APS are warranted. Disclosures: No relevant conflicts of interest to declare.

Effects of Intensive Blood Pressure Control in Patients with Evident Cardiovascular Disease: An Investigation Using the SPRINT Study Data

2019 ◽  
Vol 17 (3) ◽  
pp. 298-306 ◽  
Author(s):  
Charalambos Vlachopoulos ◽  
Dimitrios Terentes-Printzios ◽  
Konstantinos Aznaouridis ◽  
Nikolaos Ioakeimidis ◽  
Panagiotis Xaplanteris ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Beneficial Effect ◽  
Harmful Effect ◽  
Adverse Outcomes ◽  
Intensive Treatment ◽  
Serious Adverse Events ◽  
Stroke Incidence ◽  
Increased Risk ◽  
All Cause Mortality

Background: Recent data advocate adoption of a more intensive treatment strategy for management of blood pressure (BP). </P><P> Objective: We investigated whether the overall effects of the Systolic Blood Pressure Intervention Trial (SPRINT) are applicable to cardiovascular disease (CVD) patients. </P><P> Methods: In a post hoc analysis we analyzed data from SPRINT that randomly assigned 9361 individuals to a systolic BP (SBP) target of <120 mmHg (intensive treatment) or <140 mmHg (standard treatment). 1562 patients had clinically evident CVD (age=70.3±9.3 years, 24% females) at study entry and were followed for 3.1 years. Further, we assessed the effect of low (<150 mmHg) baseline SBP on outcome. </P><P> Results: In CVD patients, there was no benefit from the intensive treatment regarding all endpoints, except for a marginally significant benefit on all-cause mortality (hazard ratio [HR]: 0.67; 95% confidence interval [CI], 0.45 to 1.00; p=0.0509). Further, while there was no increase in serious adverse events (SAE) in the intensive group, there was increased risk for study-related SAE, acute renal failure and electrolyte abnormalities. In patients with low baseline SBP there was a beneficial effect on allcause mortality (HR: 0.56; 95% CI: 0.33 to 0.96; p=0.033), but with greater stroke incidence (HR: 2.94; 95% CI: 1.04 to 8.29; p=0.042). </P><P> Conclusion: We confirm the beneficial effect of the intensive strategy in SPRINT study on all-cause mortality and the harmful effect on specific adverse outcomes in patients with CVD. However, in patients with low baseline SBP stroke may increase.

Diabetes and Heart Failure: Is it Hyperglycemia or Hyperinsulinemia?

2020 ◽  
Vol 18 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Triantafyllos Didangelos ◽  
Konstantinos Kantartzis
Keyword(s):  
Heart Failure ◽  
Insulin Treatment ◽  
Close Association ◽  
Adverse Outcomes ◽  
Negative Effects ◽  
Beneficial Effects ◽  
Appropriate Treatment ◽  
Increased Risk ◽  
Treatment Of Diabetes

The cardiac effects of exogenously administered insulin for the treatment of diabetes (DM) have recently attracted much attention. In particular, it has been questioned whether insulin is the appropriate treatment for patients with type 2 diabetes mellitus and heart failure. While several old and some new studies suggested that insulin treatment has beneficial effects on the heart, recent observational studies indicate associations of insulin treatment with an increased risk of developing or worsening of pre-existing heart failure and higher mortality rates. However, there is actually little evidence that the associations of insulin administration with any adverse outcomes are causal. On the other hand, insulin clearly causes weight gain and may also cause serious episodes of hypoglycemia. Moreover, excess of insulin (hyperinsulinemia), as often seen with the use of injected insulin, seems to predispose to inflammation, hypertension, dyslipidemia, atherosclerosis, heart failure, and arrhythmias. Nevertheless, it should be stressed that most of the data concerning the effects of insulin on cardiac function derive from in vitro studies with isolated animal hearts. Therefore, the relevance of the findings of such studies for humans should be considered with caution. In the present review, we summarize the existing data about the potential positive and negative effects of insulin on the heart and attempt to answer the question whether any adverse effects of insulin or the consequences of hyperglycemia are more important and may provide a better explanation of the close association of DM with heart failure.

scholarly journals COVID-19 and cancer registries: learning from the first peak of the SARS-CoV-2 pandemic

2021 ◽  
Author(s):  
Alvin J. X. Lee ◽  
Karin Purshouse
Keyword(s):  
Risk Factors ◽  
Performance Status ◽  
Poor Performance ◽  
Cancer Registries ◽  
Adverse Outcomes ◽  
Smoking History ◽  
Poor Performance Status ◽  
International Studies ◽  
Patients With Cancer ◽  
Increased Risk

AbstractThe SARS-Cov-2 pandemic in 2020 has caused oncology teams around the world to adapt their practice in the aim of protecting patients. Early evidence from China indicated that patients with cancer, and particularly those who had recently received chemotherapy or surgery, were at increased risk of adverse outcomes following SARS-Cov-2 infection. Many registries of cancer patients infected with SARS-Cov-2 emerged during the first wave. We collate the evidence from these national and international studies and focus on the risk factors for patients with solid cancers and the contribution of systemic anti-cancer treatments (SACT—chemotherapy, immunotherapy, targeted and hormone therapy) to outcomes following SARS-Cov-2 infection. Patients with cancer infected with SARS-Cov-2 have a higher probability of death compared with patients without cancer. Common risk factors for mortality following COVID-19 include age, male sex, smoking history, number of comorbidities and poor performance status. Oncological features that may predict for worse outcomes include tumour stage, disease trajectory and lung cancer. Most studies did not identify an association between SACT and adverse outcomes. Recent data suggest that the timing of receipt of SACT may be associated with risk of mortality. Ongoing recruitment to these registries will enable us to provide evidence-based care.

Lower perception of pharmacological treatment increases risk of non-adherence to medication

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
CB Graversen ◽  
JB Valentin ◽  
ML Larsen ◽  
S Riahi ◽  
T Holmberg ◽  
...  
Keyword(s):  
Pharmacological Treatment ◽  
Poisson Regression ◽  
Drug Class ◽  
Angiotensin Receptor Blockers ◽  
Adverse Outcomes ◽  
Adherence To Medication ◽  
Increased Risk ◽  
Patient Reported ◽  
High Level

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): The Danish Heart Foundation Background A large proportion of patients fail to reach optimal adherence to medication following incident ischemic heart disease (IHD) despite amble evidence of the beneficial effect of medication. Non-adherence to medication increases risk of disease-related adverse outcomes but none has explored how perception about pharmacological treatment detail on non-adherence using register-based follow-up data. Purpose To investigate the association between patients’ perception of pharmacological treatment and risk of non-initiation and non-adherence to medication in a population with incident IHD. Methods This cohort study followed 871 patients until 365 days after incident IHD. The study combined patient-reported survey data on perception about pharmacological treatment (categorised by ‘To a high level’, ‘To some level’, and ‘To a lesser level’) with register-based data on reimbursed prescription of cardiovascular medication (antithrombotics, statins, ACE-inhibitors/angiotensin receptor blockers, and β-blockers). Non-initiation was defined as no pick-up of medication in the first 180 days following incident IHD and analysed by Poisson regression. Two different measures evaluated non-adherence in patients initiating treatment: 1) proportion of days covered (PDC) analysed by Poisson regression, and 2) risk of discontinuation analysed by Cox proportional hazard regression. All analyses were adjusted for confounding variables (age, sex, ethnicity, income, educational level, civil status, occupation, charlson comorbidity index, supportive relatives, and individual consultation in medication) identified by directed acyclic graph and obtained from national registers and the survey. Item non-response was handled by multiple imputation and item consistency was evaluated by McDonalds omega. Results Lower perceptions about pharmacological treatment was associated with increased risk of non-initiation and non-adherence to medication irrespectively of drug class and adherence measure in the multiple adjusted analyses (please see figure illustrating results on antithrombotics). A dose-response relationship was observed both at 180- and 365-days of follow-up, but the steepest decline in adherence differed when comparing the two adherence measures (results not shown). Moderate internal consistency was found for the summed measure of perception (McDonalds omega = 0.67). Conclusion Lower perception of pharmacological treatment was associated with subsequent non-initiation and non-adherence to medication, irrespectively of measurement method and drug class. Abstract Figure. Figre: Multiple adjusted analyses

scholarly journals Postoperative acute kidney injury in adult non-cardiac surgery: joint consensus report of the Acute Disease Quality Initiative and PeriOperative Quality Initiative

2021 ◽  
Author(s):  
John R. Prowle ◽  
Lui G. Forni ◽  
Max Bell ◽  
Michelle S. Chew ◽  
Mark Edwards ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Adverse Outcomes ◽  
Baseline Risk ◽  
Major Surgery ◽  
Increased Risk

AbstractPostoperative acute kidney injury (PO-AKI) is a common complication of major surgery that is strongly associated with short-term surgical complications and long-term adverse outcomes, including increased risk of chronic kidney disease, cardiovascular events and death. Risk factors for PO-AKI include older age and comorbid diseases such as chronic kidney disease and diabetes mellitus. PO-AKI is best defined as AKI occurring within 7 days of an operative intervention using the Kidney Disease Improving Global Outcomes (KDIGO) definition of AKI; however, additional prognostic information may be gained from detailed clinical assessment and other diagnostic investigations in the form of a focused kidney health assessment (KHA). Prevention of PO-AKI is largely based on identification of high baseline risk, monitoring and reduction of nephrotoxic insults, whereas treatment involves the application of a bundle of interventions to avoid secondary kidney injury and mitigate the severity of AKI. As PO-AKI is strongly associated with long-term adverse outcomes, some form of follow-up KHA is essential; however, the form and location of this will be dictated by the nature and severity of the AKI. In this Consensus Statement, we provide graded recommendations for AKI after non-cardiac surgery and highlight priorities for future research.

Short- and long-term outcomes of preterm spontaneous twin anemia-polycythemia sequence

2020 ◽  
Vol 48 (4) ◽  
pp. 329-334
Author(s):  
Soo Jin Han ◽  
Seung Mi Lee ◽  
Sohee Oh ◽  
Subeen Hong ◽  
Jeong Won Oh ◽  
...  
Keyword(s):  
Cord Blood ◽  
Neonatal Morbidity ◽  
Adverse Outcomes ◽  
Control Group ◽  
Long Term Outcomes ◽  
Neurodevelopmental Outcomes ◽  
Monochorionic Twin ◽  
Increased Risk ◽  
Study Population

AbstractBackgroundIn monochorionic twin pregnancy, placental anastomosis and inter-twin blood transfusion can result in specific complications, such as twin-twin transfusion syndrome (TTTS) and twin anemia-polycythemia sequence (TAPS). It is well established that adverse outcomes are increased in TTTS, but reports on the neonatal and long-term outcomes of TAPS are lacking. The objective of this study was to evaluate the neonatal and neurodevelopmental outcomes in spontaneous TAPS.MethodsThe study population consisted of monochorionic twin pregnancies with preterm birth (24–37 weeks of gestation) between November 2003 and December 2016 and in which cord blood was taken at the time of delivery. According to the result of hemoglobin in cord blood, the study population was divided into two groups: a spontaneous TAPS group and a control group. Neonatal and neurodevelopmental outcomes were compared between the two groups.ResultsDuring the study period, 11 cases were diagnosed as spontaneous TAPS (6.4%). The TAPS group had lower gestational age at delivery and had a higher risk for cesarean delivery. However, neonates with TAPS were not at an increased risk for neonatal mortality and significant neonatal morbidity. In addition, the frequency of severe cerebral lesion during the neonatal period and the risk of cerebral palsy at 2 years of age were not different between the two groups.ConclusionThe spontaneous TAPS diagnosed by postnatal diagnostic criteria was not associated with the increased risk of adverse neonatal and neurodevelopmental outcomes. Further studies are needed to evaluate the morbidity of antenatally diagnosed TAPS.

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