Coagulation Derangements Research Articles

Cancer-Related Coagulopathy and Perioperative Considerations.

Cancer-related coagulation abnormalities are characterized by complex dysregulation of the hemostatic system, predisposing patients to increased risk of thrombotic and hemorrhagic complications and associated increased morbidity and mortality. Advances in anticancer therapies with improved outcomes have led to better survival and older age of patients living with or having survived cancer. There is also a significant increase in the number of patients diagnosed with cancer. All these factors will increase the number of patients presenting for surgical procedures, both cancer-related and noncancer related. It is important for the anesthesiologist to understand the magnitude of cancer-related coagulation derangement, its types, pathophysiology, and clinical presentation, to optimize the perioperative management of this high-risk rapidly growing patient population.

Hemostasis and thrombosis risks and management in vascular anomalies.

The role of the hematologist in the management of vascular anomalies is evolving. Several vascular tumors and malformations are associated with complex coagulation derangements. Kaposiform hemangioendothelioma or tufted angiomas may present with a consumptive coagulopathy known as the Kasabach-Merritt phenomenon (KMP). The management of KMP is essential to reduce morbidity and mortality from this condition. Slow-flow vascular malformations (SFVM) are also frequently complicated by a coagulopathy requiring anticoagulation, especially during and after surgical procedures, and some of these conditions pose a high risk of venous thromboembolism. Pain in SFVM is also frequently responsive to anticoagulation as well. It is essential for a hematologist with expertise in vascular anomalies to assist in the management of these complex conditions as part of a multidisciplinary team to reduce morbidity and mortality. Through case-based discussions, we attempt to highlight the critical role of the hematologist in managing these anomalies.

Systemic Coagulation Derangement as an Early Sign of Oxygenator Failure in Veno-Venous Extracorporeal Membrane Oxygenation (VV ECMO) Without Anticoagulation

Background and Clinical Significance: Veno-venous extracorporeal membrane oxygenation (VV ECMO) has become a widely accepted supportive treatment for severe acute respiratory distress syndrome (ARDS) in intensive care units (ICUs). Although it has gained popularity, some of its aspects, including optimal anticoagulation management and the best means of monitoring hemostasis, remain unresolved. Thrombosis and bleeding are still important complications of ECMO. Case Presentation: A 44-year-old male patient, with no underlying conditions, was diagnosed with severe acute respiratory distress syndrome (ARDS) due to AH1N1 influenza. He presented severe hypoxemia despite the use of mechanical ventilation, neuromuscular blocking agent infusion and prone position. VV ECMO was used, and coagulation was stopped on ECLS day 6 due to severe pulmonary hemorrhage. The systemic hemostatic disorders found in this patient were difficult to differentiate from disseminated intravascular coagulation (DIC) or sepsis-induced coagulopathy (SIC), improved transiently after circuit exchange, and resolved only after discontinuation of ECMO. The patient was discharged fully conscious and cooperative, with no apparent neurological deficit. Conclusions: Systemic hemostatic abnormalities may precede oxygenator failure and mimic DIC or SIC. Timely oxygenator exchange may therefore be considered. However, it is a high-risk procedure, especially in fully ECLS-dependent patients.

Serum from patients with cirrhosis undergoing liver transplantation induces permeability in human pulmonary microvascular endothelial cells ex vivo.

Patients with cirrhosis undergoing liver transplantation frequently exhibit systemic inflammation, coagulation derangements, and edema, indicating endothelial dysfunction. This syndrome may worsen after ischemia-reperfusion injury of the liver graft, coincident with organ dysfunction that worsens patient outcomes. Little is known about changes in endothelial permeability during liver transplantation. We hypothesized that sera from these patients would increase permeability in cultured human endothelial cells ex vivo. Adults with cirrhosis presenting for liver transplantation provided consent for blood collection during surgery. Sera were prepared at five time points spanning the entire operation. The barrier function of human pulmonary microvascular endothelial cells in culture was assessed by transendothelial resistance measured using the ECIS ZΘ system. Confluent cells from two different endothelial cell donors were stimulated with human serum from liver transplant patients. Pooled serum from healthy men and purified inflammatory agonists served as controls. The permeability response to serum was quantified as the area under the normalized resistance curve. Responses were compared between time points and analyzed for associations with clinical characteristics of liver transplant patients and their grafts. Liver transplant sera from all time points during surgery-induced permeability in both endothelial cell lines. The magnitude of permeability change was heterogeneous between patients, and there were differences in the effects of sera on the two endothelial cell lines. In one of the cell lines, the severity of liver disease was associated with greater permeability at the start of surgery. In the same cell line, serum collected 15 min after liver reperfusion induced significantly more permeability as compared to that collected at the start of surgery. Early postreperfusion sera from patients undergoing living donor transplants induced more permeability than sera from deceased donor transplants. Sera from two exemplary cases of patients on preoperative dialysis, and one patient with an unexpectedly long warm ischemia time of the liver graft, induced exaggerated and prolonged endothelial permeability. Serum from patients with cirrhosis undergoing liver transplantation induces permeability of cultured human pulmonary microvascular endothelial cells. Increased endothelial permeability during liver transplantation may contribute to organ injury and present a target for future therapeutics.

Early Infantile Hemophagocytic Lymphohistiocytosis Masquerading as Late-onset Sepsis: A Case Report with Review of the Literature

Background: Hemophagocytic lymphohistiocytosis (HLH) is a condition due to uncontrolled overactivation of macrophages, cytotoxic T cells, and natural killer cells creating a cytokine storm, characterized by multiorgan involvement. Familial HLH (fHLH) is due to genetic defects and presents early in life. There are only a few reports of neonatal onset of fHLH. Clinical Description: A 40-days-old male baby, born at 36 weeks of gestation, presented with fever, abdominal distension, poor feeding, lethargy, seizures. He had metabolic acidosis, respiratory failure, hepatosplenomegaly and bicytopenia, with a deranged coagulation profile. Management and Outcome: Treatment was started as per sepsis with meningitis with disseminated coagulation profile. All cultures were sterile, bacterial and fungal polymerase chain reaction were negative, but the baby deteriorated rapidly to shock. As the baby fulfilled the HLH criteria, he was started on intravenous immunoglobulin, methylprednisolone, and immunomodulator anakinra while sending sample for whole-exome sequencing for primary HLH. However, the baby succumbed to the illness. Whole-exome sequencing revealed a perforin-1 gene defect which confirmed primary HLH type 2. Conclusion: This report creates awareness that a primary genetic HLH may mimic early infantile sepsis. The rapidly progressive course in an otherwise healthy, breast-fed baby, with no setting of sepsis, and absence of infective etiology, should raise a suspicion of this underlying potentially fatal condition.

A case series of forearm compartment syndrome complicating transradial cardiac catheterization

BackgroundAcute compartment syndrome following a transradial coronary approach is rare. However, as the incidence of coronary arterial disease increases due to lifestyle factors and multiple comorbidities, transradial coronary angiography has become more common for diagnostic and therapeutic purposes in cardiovascular centers. Despite its rarity, we encountered two cases of acute compartment syndrome within a 1-week interval in the cardiology unit of a tertiary hospital.Case presentationThe first case involved a 75-year-old woman diagnosed with non-ST elevation myocardial infarction (NSTEMI). A coronary angiogram was performed via an uncomplicated right radial artery puncture. Following the procedure, the patient experienced significant swelling in the right forearm. An emergency fasciotomy release of the right forearm was conducted, revealing a gushing hematoma upon entering the flexor compartment. Fortunately, the wound healed well two months postoperatively with no functional deficits. In the second case, an 80-year-old man presented with severe angina pectoris upon exertion and was diagnosed with NSTEMI. The following day, he developed compartment syndrome in the left forearm, necessitating an emergency fasciotomy. Intraoperative examination revealed muscle bulging within the forearm compartments accompanied by extensive hematoma. Postoperatively, a deranged coagulation profile caused oozing from the wound. However, since there was no arterial bleeding, a compression dressing was applied. This led to a gradual drop in hemoglobin levels and worsened his heart condition. Despite resuscitative efforts and attempts to correct the coagulopathy, the patient experienced cardiorespiratory arrest and succumbed to ischemic heart disease in failure.ConclusionClinicians must remain vigilant in identifying this potentially limb-threatening condition. Patients with pre-existing anticoagulant therapy and underlying atherosclerotic disease are at a higher risk of bleeding complications. Implementing effective hemostasis techniques and promptly managing swelling can help prevent the occurrence of compartment syndrome. Timely assessment and maintaining a high level of clinical suspicion are paramount. If necessary, early consideration of decompressive fasciotomy is essential to avert catastrophic outcomes.

Complete blood count, coagulation biomarkers, and lung function 6 months after critical COVID-19.

Understanding the recovery of post-COVID-19 organ dysfunction is essential. We evaluated coagulation 6 months post-COVID-19, examining its recovery and association with lung function. Patients treated for COVID-19 at intensive care units between 3/2020 and 1/2021 were analyzed for complete blood count (CBC) and coagulation biomarkers (prothrombin time activity (%) (PT%), activated partial thromboplastin time (APTT), fibrinogen, coagulation factor VIII (FVIII), antithrombin (AT), and D-dimer) during the 6 months post-hospitalization. Results were compared with acute phase values and correlated with pulmonary function tests (PFT), including forced vital capacity (FVC) and hemoglobin-corrected diffusing capacity percentage of predicted (DLCOc%), recorded 6 months post-hospitalization. We examined the association between coagulation biomarkers and DLCOc% using linear regression with age, sex, and invasive mechanical ventilation (IMV) duration, and FVIII (correlated with DLCOc%) as covariates. Most CBCs and coagulation biomarkers had median values within the normal range. However, only 21% (15/70) of patients achieved full normalization of all biomarkers. Compared to acute COVID-19, hemoglobin, PT%, and AT increased, while leukocytes, fibrinogen, FVIII, and D-dimer decreased. Despite decreased levels, FVIII remained elevated in 46% (31/68), leukocytes in 26% (18/70), and D-dimer in 27% (18/67) at 6 months. A weak negative correlation (r = -0.37, p = .036) was found between DLCOc% and FVIII. Multivariable analysis revealed a weak, independent association between DLCOc% and FVIII. Excluding patients with anticoagulation therapy, FVIII no longer correlated with DLCOc%, while AT showed a moderate correlation with DLCOc%. Only a few patients had normal CBC and coagulation biomarker values 6 months after critical COVID-19. A weak negative correlation between DLCOc% and FVIII suggests that deranged coagulation activity may be associated with reduced diffusing capacity.

Impella as Bridge to Durable Left Ventricular Assist Device in Acute Myocardial Infarction Cardiogenic Shock Patients.

Implantation of durable left ventricular assist device (LVAD) in cardiogenic shock (CS) patients after acute myocardial infarction (AMI) poses specific challenges (small left ventricular size, acute infarct area, need for antithrombotic therapy, status Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) 1 with impaired organ function and derangements in coagulation and inflammatory parameters) which may affect outcomes. We reviewed data of all AMI-CS patients who were implanted LVAD after Impella support at a referral center with the aim to analyze feasibility, timing, and outcomes of durable LVAD implantation after tMCS with Impella due to AMI-CS. Twenty-one patients were treated between 2013 and 2023: all were in Society for Cardiovascular Angiography & Interventions (SCAI) class D-E and INTERMACS 1-2 at presentation, median LV ejection fraction (EF) and LV end-diastolic diameter (EDD) were 15 (10-20)% and 57 (54-60) mm, respectively. Eleven patients (52%) were supported with Impella CP, seven with Impella 5.0 (33%), and three (14%) with Impella 2.5. Axillary cannulation was performed in nine patients (43%). Five patients (24%) had concomitant venoarterial extracorporeal membrane oxygenation (VA-ECMO) support. Median duration of Impella support was 12 (8-14) days. Overall, the use of Impella was characterized by low rate of complications and allowed successful bridge to durable LVAD in all patients, with 100% 30 day survival rate.

Case of Autoimmune Haemolytic Anaemia (Aiha) in an Immunocompetent 1-Month-Old Child with Congenital Cytomegalovirus (cCMV) Infection

Here we report a case of congenital CMV infection with rare presentation as haemolytic anaemia in a 50-day-old infant. Clinical manifestations of our patient were pallor, jaundice, hepatosplenomegaly, and a deranged coagulation profile. Congenital CMV being the most common viral congenital infection should be suspected in every neonate and infant presenting with haemolytic anaemia. It is also the most common non-genetic cause of SNHL and not much is yet there for its prevention except for primary prevention as the role of immunoglobulin is still under trial.

Case of Covid-19 co-infection with Crimean Congo haemorrhagic fever (CCHF) in a CCHF endemic country: a case report

Covid-19 pandemic affected the health care systems globally. In many countries, healthcare services were overwhelmed by the huge number of Covid cases; hence, shifting the focus from locally endemic infectious diseases. Such a case presented to us that was initially managed along the lines of critical Covid pneumonia with steroids, Remdesivir, and supplemental oxygen for hypoxic respiratory failure. The patient also received Baricitinib, to which he was non-responsive and thus offered invasive mechanical ventilation. Post intubation, the patient was managed for Covid-associated ARDS with lung protective ventilation. He later also developed liver dysfunction, renal failure, coagulation derangements, and shock. Workup for malaria and dengue were negative. Later, Crimean Congo PCR was sent which came positive; a possible cause of progressive deterioration. In CCHF endemic areas, it is crucial to rule out the CCHF infection among patients presenting with critical Covid pneumonia due to similar clinical presentation in both the infections.

Factor V Inhibitor in COVID-19 an Unusual Presentation

Introduction : A huge variety of haematological manifestations and derangements have been frequently published with COVID-19 infections, however Factor V deficiency and COVID-19 infection has not been documented. We are reporting a case of acquired Factor V deficiency due to inhibitor caused by COVID 19 infection . Factor V deficiency is a rare bleeding disorder having either inherited or acquired forms. Acquired factor V deficiency (AFVD) can present at any age, with the manifestations ranging from abnormal deranged PT/PTT to serious bleeding and quite often challenging to diagnose. The risk factors for development of inhibitors include surgical procedures, Hepatitis, antibiotic, Urinary tract infections, blood transfusions, haemodialysis, malignancies like multiple myeloma, amyloidosis and autoimmune disorders. Around 30% of cases of AFVI are found to be idiopathic. Studies suggest that there is a temporal Connection between SARS-CoV-2 infection and the development of coagulopathy. This could be possible since COVID -19 infection is well associated with autoimmune coagulation abnormalities such as lupus anticoagulant, antiphospholipid antibodies, and venous thromboembolism. The precise mechanisms behind the relationship between Covid19 infection and development of Factor V deficiency is not fully understood. SARS-CoV-2 infection induces a proinflammatory state causing endothelial damage, platelet activation and hyperviscosity. We suggest that the factor V inhibitor was formed in the setting of immune dysregulation from the underlying COVID-19 as coagulation profile was normal before admission to hospital. Result and method: A 62 year old gentleman with background of dyslipidemia and IBS was admitted to the hospital with asymptomatic COVID pneumonia. The patient was started on Lopinavir-Ritonivir 500mg BID and enoxaparin 40mg OD. Upon routine testing patient was found to have a deranged coagulation profile (PT: 41.9sec/APTT: 104.7sec/INR: 3.5/Fibrinogen: 3.04gm/L/ D-dimer: <0.30mg/L FEU). Daily results kept showing a steady rise of coagulation parameters (PT: 46.5sec/APTT: 122.0sec/INR: 3.9) however the patient was asymptomatic. Results demonstrated severe factor V deficiency (<5.7%) with mildly reduced Factor VII (53.8%) and a mildly elevated factor VIII (195.4%). PT and APTT mixing studies showed no correction of the prolonged clotting times before and after 2 hours incubation, hence the failure of correction suggested the presence of an inhibitor for which Bethesda test for Inhibitor's titer and autoimmune screening were sent. Considering the Factor V inhibitor deficiency with background of active COVID-19 infection and to prevent bleeding complications, the patient was started on Inhibitor eradication therapy with Dexamethasone 20 mg, and Immune globulin intravenous 45 gm. Inhibitor titers came back positive for an inhibitor level of 9 BU/ml. Autoimmune screen for ANA and anti-B2 glycoprotein came back negative. Malignancy was ruled out. Throughout the hospital stay , we did not encounter any bleeding manisfestions or drop in haemoglobin. Since the patient had a previous record of normal coagulation profile in 2019, a diagnosis of COVID-19 infection-related Factor V deficiency with inhibitor was made. After a four-days course of inhibitors eradication, PT INR and aPTT started coming down with no significant complications, the patient was discharged on oral prednisolone and vitamin K. Follow up in the clinic after 3 weeks showed complete normalization of coagulation profile. Conclusion: A wide range of haematological manifestation have been reported with COVID-19 infection, but the association of Factor V deficiency due to inhibitors and COVID-19 infection have not been reported in the literature earlier. Treatment will be focusing on treating the primary cause and eradication of the inhibitors.

The nature and timing of coagulation dysfunction in a cohort of trauma patients in the Australian pre-hospital setting

BackgroundAcute Traumatic Coagulopathy (ATC) is a complex pathological process that is associated with patient mortality and increased blood transfusion requirements. It is evident on hospital arrival, but there is a paucity of information about the nature of ATC and the characteristics of patients that develop ATC in the pre-hospital setting. The objective of this study was to describe the nature and timing of coagulation dysfunction in a cohort of injured patients and to report on patient and pre-hospital factors associated with the development of ATC in the field. MethodsThis was a prospective observational study of a convenience sample of trauma patients. Patients had blood taken during the pre-hospital phase of care and evaluated for derangements in Conventional Coagulation Assays (CCA) and Rotational Thromboelastometry (ROTEM). Associations between coagulation derangement and pre-hospital factors and patient outcomes were evaluated. ResultsA total of 216 patients who had either a complete CCA or ROTEM were included in the analysis. One hundred and eighty (83 %) of patients were male, with a median injury severity score of 17 [interquartile range (IQR) 10–27] and median age of 34 years [IQR = 25.0–52.0]. Hypofibrinogenemia was the predominant abnormality seen, (CCA Hypofibrinogenemia: 51/193, 26 %; ROTEM hypofibrinogenemia: 65/204, 32 %). Increased CCA derangement, the presence of ROTEM coagulopathy, worsening INR, worsening FibTEM and decreasing fibrinogen concentration, were all associated with both mortality and early massive transfusion. ConclusionClinically significant, multifaceted coagulopathy develops early in the clinical course, with hypofibrinogenemia being the predominant coagulopathy. In keeping with the ED literature, pre-hospital coagulation dysfunction was associated with mortality and early massive transfusion. Further work is required to identify strategies to identify and guide the pre-hospital management of the coagulation dysfunction seen in trauma.

Trauma-induced coagulopathy: What you need to know.

Trauma-induced coagulopathy (TIC) is a global inflammatory state accompanied by coagulation derangements, acidemia, and hypothermia, which occurs after traumatic injury. It occurs in approximately 25% of severely injured patients, and its incidence is directly related to injury severity. The mechanism of TIC is multifaceted; proposed contributing factors include dysregulation of activated protein C, increased tPA, systemic endothelial activation, decreased fibrinogen, clotting factor consumption, and platelet dysfunction. Effects of TIC include systemic inflammation, coagulation derangements, acidemia, and hypothermia. Trauma-induced coagulopathy may be diagnosed by conventional coagulation tests including platelet count, Clauss assay, international normalized ratio, thrombin time, prothrombin time, and activated partial thromboplastin time; viscoelastic hemostatic assays such as thrombelastography and rotational thrombelastography; or a clinical scoring system known as the Trauma Induced Coagulopathy Clinical Score. Preventing TIC begins in the prehospital phase with early hemorrhage control, blood product resuscitation, and tranexamic acid therapy. Early administration of prothrombin complex concentrate is also being studied in the prehospital environment. The mainstays of TIC treatment include hemorrhage control, blood and component transfusions, and correction of abnormalities such as hypocalcemia, acidosis, and hypothermia. Therapeutic/Care Management; Level III.

Early and Empirical High-Dose Cryoprecipitate for Hemorrhage After Traumatic Injury

Critical bleeding is associated with a high mortality rate in patients with trauma. Hemorrhage is exacerbated by a complex derangement of coagulation, including an acute fibrinogen deficiency. Management is fibrinogen replacement with cryoprecipitate transfusions or fibrinogen concentrate, usually administered relatively late during hemorrhage. To assess whether survival could be improved by administering an early and empirical high dose of cryoprecipitate to all patients with trauma and bleeding that required activation of a major hemorrhage protocol. CRYOSTAT-2 was an interventional, randomized, open-label, parallel-group controlled, international, multicenter study. Patients were enrolled at 26 UK and US major trauma centers from August 2017 to November 2021. Eligible patients were injured adults requiring activation of the hospital's major hemorrhage protocol with evidence of active hemorrhage, systolic blood pressure less than 90 mm Hg at any time, and receiving at least 1 U of a blood component transfusion. Patients were randomly assigned (in a 1:1 ratio) to receive standard care, which was the local major hemorrhage protocol (reviewed for guideline adherence), or cryoprecipitate, in which 3 pools of cryoprecipitate (6-g fibrinogen equivalent) were to be administered in addition to standard care within 90 minutes of randomization and 3 hours of injury. The primary outcome was all-cause mortality at 28 days in the intention-to-treat population. Among 1604 eligible patients, 799 were randomized to the cryoprecipitate group and 805 to the standard care group. Missing primary outcome data occurred in 73 patients (principally due to withdrawal of consent) and 1531 (95%) were included in the primary analysis population. The median (IQR) age of participants was 39 (26-55) years, 1251 (79%) were men, median (IQR) Injury Severity Score was 29 (18-43), 36% had penetrating injury, and 33% had systolic blood pressure less than 90 mm Hg at hospital arrival. All-cause 28-day mortality in the intention-to-treat population was 26.1% in the standard care group vs 25.3% in the cryoprecipitate group (odds ratio, 0.96 [95% CI, 0.75-1.23]; P = .74). There was no difference in safety outcomes or incidence of thrombotic events in the standard care vs cryoprecipitate group (12.9% vs 12.7%). Among patients with trauma and bleeding who required activation of a major hemorrhage protocol, the addition of early and empirical high-dose cryoprecipitate to standard care did not improve all cause 28-day mortality. ClinicalTrials.gov Identifier: NCT04704869; ISRCTN Identifier: ISRCTN14998314.

Principal component analysis of a swine injury model identifies multiple phenotypes in trauma.

Trauma is the third leading cause of death in the United States and the primary cause of death for people between the ages of 1 year and 44 years. In addition to tissue damage, trauma may also activate an inflammatory state known as trauma-induced coagulopathy (TIC) that is associated with clotting malfunctions, acidemia, and end-organ dysfunction. Prior work has also demonstrated benefit to acknowledging the type and severity of endothelial injury, coagulation derangements, and systemic inflammation in the management of trauma patients. This study builds upon prior work by combining laboratory, metabolic, and clinical metrics into an analysis of trauma phenotypes, evolution of phenotypes over time after trauma, and significance of trauma phenotype on mortality. Seventy 3-month-old female Yorkshire crossbred swine were randomized to injury and resuscitation groups. Principal component analysis (PCA) of longitudinal swine TEG data (Reaction time, Alpha-Angle, Maximum Amplitude, and Clot Lysis at 30 minutes), pH, lactate, and MAP was completed in R at baseline, 1 hour postinjury, 3 hours postinjury, 6 hours postinjury, and 12 hours postinjury. Subjects were compared by principal component factor scores to assess differences in survival, injury severity, and treatment group. Among injured animals, three phenotypes were observed at each time point. Five phenotypes were associated with differences in survival, and of these, four were associated with differences in injury severity. Phenotype alignment was not significantly different by treatment group. This application of PCA to a set of coagulation, hemodynamic, and organ perfusion variables has identified multiple evolving phenotypes after trauma. Some of these phenotypes may correlate with injury severity and may have implications for survival. Next steps include validating these findings over greater numbers of subjects and exploring other machine-learning techniques for phenotype identification. Level IV, Therapeutic/Care Management.

Thrombotic and hemorrhagic complications of COVID-19 in adults hospitalized in high-income countries compared with those in adults hospitalized in low- and middle-income countries in an international registry

BackgroundCOVID-19 has been associated with a broad range of thromboembolic, ischemic, and hemorrhagic complications (coagulopathy complications). Most studies have focused on patients with severe disease from high-income countries (HICs). ObjectivesThe main aims were to compare the frequency of coagulopathy complications in developing countries (low- and middle-income countries [LMICs]) with those in HICs, delineate the frequency across a range of treatment levels, and determine associations with in-hospital mortality. MethodsAdult patients enrolled in an observational, multinational registry, the International Severe Acute Respiratory and Emerging Infections COVID-19 study, between January 1, 2020, and September 15, 2021, met inclusion criteria, including admission to a hospital for laboratory-confirmed, acute COVID-19 and data on complications and survival. The advanced-treatment cohort received care, such as admission to the intensive care unit, mechanical ventilation, or inotropes or vasopressors; the basic-treatment cohort did not receive any of these interventions. ResultsThe study population included 495,682 patients from 52 countries, with 63% from LMICs and 85% in the basic treatment cohort. The frequency of coagulopathy complications was higher in HICs (0.76%-3.4%) than in LMICs (0.09%-1.22%). Complications were more frequent in the advanced-treatment cohort than in the basic-treatment cohort. Coagulopathy complications were associated with increased in-hospital mortality (odds ratio, 1.58; 95% CI, 1.52-1.64). The increased mortality associated with these complications was higher in LMICs (58.5%) than in HICs (35.4%). After controlling for coagulopathy complications, treatment intensity, and multiple other factors, the mortality was higher among patients in LMICs than among patients in HICs (odds ratio, 1.45; 95% CI, 1.39-1.51). ConclusionIn a large, international registry of patients hospitalized for COVID-19, coagulopathy complications were more frequent in HICs than in LMICs (developing countries). Increased mortality associated with coagulopathy complications was of a greater magnitude among patients in LMICs. Additional research is needed regarding timely diagnosis of and intervention for coagulation derangements associated with COVID-19, particularly for limited-resource settings.

PERIOPERATIVE MANAGEMENT OF A CARCINOMA OF STOMACH CASE PRESENTING WITH GASTRIC OUTLET SYNDROME AND RECENT MYOCARDIAL INFARCTION-ASSESSMENT, RISK STRATIFICATION, OPTIMISATION AND ANAESTHETIC MANAGEMENT

The patients with perioperative myocardial infarction (PMI) have increased risk of myocardial ischemia, myocardial infarction (MI), conduction disturbances, cardiac failure, morbidity and mortality. The risks of these events are even higher in patients with recent MI. Here, we report 53year old female diagnosed with carcinoma of stomach presenting with gastric outlet obstruction symptoms. The surgery planned was distal gastrectemy, lymhadenectomy and feeding jejunostomy. During preoperative assessment detailed history, physical examination was carried out. She gave a history of chest discomfort and breathlessness along with presenting complaints. Her ECG showed ST/T wave changes. Cardiologist opinion was obtained. The Troponin I was positive. A diagnosis of NSTMI was made. The Echocardiogram revealed Ejection Fraction of 45% and regional wall motion abnormality. She was started on blood thinners, unfractionated heparin, anti-angina drugs, anti diuretics, beta blockers and statins .The cardiologist gave moderate to high risk for surgery. The deranged coagulation parameters and electrolyte imbalance were corrected. The blood thinners were stopped ve days before surgery. Anaesthesiologist reviewed the patient and gave tness for surgery under ASA classication IV. A high risk written informed consent, repeat serum electrolytes, coagulation prole and 12 lead ECG on day of surgery were asked. Heparin was stopped 4-6 hours before surgery. Patient underwent a high risk procedure (calculated RCRI of ≥ 2) with an elevated risk of adverse perioperative cardiac outcome (MACE-moderate risk score). The perioperative management of this patient is reported

Effect of Hypoxic Ischaemic Encephalopathy on Coagulation Profile in Neonates in a Tertiary Care Center, Agra- A Prospective Clinical Study

Introduction: Perinatal asphyxia is very common in developing countries. Coagulopathy occurs as a part of spectrum of multiorgan dysfunction following hypoxic insult. In asphyxiated neonate, bleeding due to coagulation abnormality is common and potentially life threatening. There are very few studies done on coagulation profile with perinatal asphyxia in last few decades. Aim: To evaluate the coagulation profile in neonates with hypoxic ischaemic encephalopathy in a tertiary care center, Agra. Materials and Methods: This was a prospective clinical study undertaken in Neonatal Intensive Care Unit (NICU) FH Medical College Agra, a tertiary care center catering rural and urban population. Total 60 neonates admitted with history of birth asphyxia between January 2022 to June 2022 were enrolled. Neonates were classified into Hypoxic Ischaemic Encephalopathy (HIE) stage 1, 2 and 3 (according to Sarnat and Sarnat staging). Parameters such as Prothrombin Time (PT)/ International Normalised Ratio (INR) and platelet count was analysed. For describing continuous variables means and standard deviations and for comparison Analysis of Variance (ANOVA) test and Chi-square test were used. Results: In this study, total 60 neonates were enrolled. Out of these 43 (71.61%) were male and 17 (28.33%) female. Highest number of cases 34 (56.7%) were from HIE stage 3 followed by 22 (36.7%) HIE stage 2 and 4 (6.7%) from HIE stage 1. Among them 14 newborns with HIE stage 3 were died. PT and INR was significantly deranged in HIE stage 3 and 2 (p-value <0.05). HIE stage 3 has highest mortality and morbidity. Platelet count were normal in HIE stage 1 followed by decreased in HIE stage 2 and 3 and also statistically significant. Conclusion: Coagulation derangement is very common in babies with HIE and evident before clinical bleeding and this derangement is associated with poor outcome. Hence, timely intervention and appropriate management can improve the clinical outcome.

Coagulation Profile in Patients with Autoimmune Thyroiditis: A Cross-sectional Exploratory Study

Abstract Background: The association between the hemostatic system and thyroid diseases is a subject of investigation that can shed light on various abnormalities ranging from subclinical laboratory findings to thromboembolic events. Aim: The aim of this study was to evaluate the potential association between various thyroid disorders and coagulation profiles in patients with no apparent bleeding abnormalities. Materials and Methods: An analytical case–control study was carried out between April 2020 and November 2021. Adults presenting with symptoms suggestive of thyroid dysfunction/palpable goiter without any apparent bleeding disorder were included in the study. Thyroid function tests were categorized as euthyroid, hyperthyroid, and hypothyroid. Antithyroid antibodies, prothrombin time, activated partial thromboplastin time, fibrinogen, factor VIII, and D-dimer were assessed. Comparison of cases and controls and between various subgroups of cases was carried out by Student’ t-test and P ≤ 0.05 was considered significant. Results: We recruited 20 controls and 46 cases, including 18 with overt hypothyroidism, 13 with overt hyperthyroidism, 3 with subclinical hyperthyroidism, and 12 with subclinical hypothyroidism. On comparison with controls, those with overt hypothyroidism showed a hypocoagulable state with decreased fibrinogen, factor VIII, and raised D-dimer values. The converse was true in patients with hyperthyroidism and subclinical hypothyroidism, both, showing a hypercoagulable state. Only factor VIII and fibrinogen values showed statistically significant differences (P ≤ 0.05 for both) between the subgroups of cases and between those who were antibody-positive versus negative. Conclusion: Our findings support the assertion that there is a deranged coagulation profile in autoimmune thyroiditis.

ARTERIAL THROMBOSIS- A COMPLICATION OF COVID-19 PNEUMONIA: A CASE SERIES REPORT

Since the outbreak of COVID-19 virus infection in December 2019, the virus has rapidly spread across the globe causing pandemic. A variety of vascular complications have been associated with novel COVID-19 virus infection such as venous and arterial thromboembolism. Arterial thrombosis is a recognized complication of COVID -19 pneumonia suggesting the possibility of deranged coagulation profile induced by the COVID-19 virus. Arterial thrombosis can be both early and delayed manifestation of COVID-19 infection with varying presentation depending on the system involved and it can occur in patients with or without comorbidities thus prompting physicians for its early diagnosis, management and reduction of associated complications. We discuss six cases of COVID-19 patients with pulmonary and systemic arterial thrombosis with varying presentations.