Immuno-thrombosis is often described as the dysregulated interaction between innate immunity and coagulation (30–32). A reported 30-80% of COVID-19 ICU patients endure thrombotic complications during their clinical course (33–36). The most common thrombotic complication in COVID-19 patients is VTE, which occurs in 15-85% of patients (37). Although the exact mechanism behind CAC is poorly understood, endotheliitis likely incites the hypercoagulable state (Figure 2) (38–42). The SARS-CoV-2 virus directly invades endothelial cells through the angiotensin converting enzyme 2 (ACE2) receptor. This leads to localization of viral inclusion bodies in the lungs, liver, small intestines, and kidneys, shedding of endothelial glycocalyx proteins, and decreases in the level of heparanase-2. This results in a progression from normal hemostasis to a relatively antifibrinolytic state (31, 38, 43–45). The SARS-CoV-2 viral saturation of ACE2 increases circulating levels of angiotensin II, leading to increased production of the important antifibrinolytic mediator, plasminogen activator inhibitor 1 (PAI-1) (46–48). Elevated PAI-1 and thrombin-activatable fibrinolysis inhibitor (TAFI) levels in the alveolar space have been identified in COVID-19 patients (46, 49–51). Elevated tissue plasminogen activator (tPa) levels have also been noted in COVID-19 patients. This tPa release may be due to malperfusion secondary to microvascular fibrin deposition. Despite this increase in tPa, pro-thrombosis persists in these patients, suggesting that elevated PAI-1 and TAFI overwhelm the action of tPa, resulting in microvascular deposition of fibrin (52). These factors contribute to the disruption of the tightly regulated balance between thrombosis and fibrinolysis in COVID-19 patients, leading to what is known as “fibrinolytic shutdown” (17, 46, 50, 52–58). When combined with elevated thrombin generation, it leads to adverse complications such as a type of adult respiratory distress syndrome (ARDS), multisystem organ failure, and mortality (29, 59–62). This unique type of ARDS is often associated with a localized hypercoagulability of the pulmonary vasculature due to abnormal deposition of fibrin and development of microthrombosis (63–66). Postmortem analyses confirm a similar presentation in patients with COVID-19-induced ARDS (67–70). This localized hypercoagulability is partially induced by inflammation of tissue, leading to elevated tissue factor (TF) production by epithelial cells and alveolar macrophages which results in the deposition of fibrin and the development of microthrombosis (46, 71). Thromboses are additionally potentiated by a deficient fibrinolytic response primarily induced by the overexpression of PAI-1 from activated platelets and endothelial cells (31, 72, 73).

Primary hemostasis, which is accomplished via activated platelets at the site of endothelial injury, contributes to the hypercoagulable state of the COVID-19 patient. Overwhelming platelet activation is driven by many stimuli, and significantly facilitated by increased levels of von Willebrand Factor (VWF), as well as activation of the enzymatic (intrinsic) clotting pathway. COVID-19 patients have increased activation of circulating platelets as demonstrated by elevated soluble P-selectin as well as markers for endothelial activation (74). A direct stimulatory role of SARS-CoV-2 Spike protein on the COVID-19 patient’s platelets has also been described (75). Severe COVID-19 illness correlates not just with platelet activation but is also associated with enhanced platelet-monocyte aggregation. Finally, ICU admitted COVID-19 patients’ platelets induce P-selectin and αIIb/β3-dependent monocyte TF expression which may augment inflammation and hypercoagulability (76).

Together, these aberrancies in hemostasis mediated by platelets and reduced fibrinolysis (documented by whole blood viscoelastic hemostatic assays [VHAs], thromboelastography [TEG] and rotational thromboelastometry [ROTEM]) inevitably lead to uncontrollable hypercoagulopathy (76–78). The TEG/ROTEM evaluates the patient’s position along the hemostatic spectrum from hypo to hypercoagulable states. The tracings resemble a shovel, whereby the length of the handle reflects coagulation factor competence, the slope of the blade reflects fibrinogen concentration, the thickness of the blade reflects clot contraction mediated by fibrin-platelet interaction, and the tapering end of the blade represents fibrinolysis. Therefore, a characteristic early COVID-19 patient with a hypercoagulable state presents with a short handle, a steep slope, and a thick blade with no tapering of the blade, which represents enhanced effect of coagulation factors, increased fibrinogen concentration, increased fibrin/platelet function, and fibrinolytic shutdown. At the other end of the spectrum lies the hypocoagulable state as manifested by a long handle, flat slope, thin blade, with significant tapering. In Figure 3, examples of this paradigm are represented along various stages of this spectrum of coagulopathies associated with COVID-19.

The hypercoagulability of COVID-19 patients is clearly complex and multifactorial, but understanding these complex mechanisms allows for the pursuit of specific treatment strategies to improve patient outcomes. Management is complicated because of fibrinolytic shutdown due to the reduction of natural fibrinolysis at the level of the endothelium. While a multitude of studies have shown the detrimental effect of fibrinolytic shutdown on COVID-19 patient outcomes, bleeding complications such as gastrointestinal bleeding and hemorrhagic stroke are also common, especially in patients on therapeutic anticoagulation (17, 79, 80, 82–86). These patients tend to clot and bleed at the same time, a function of the “rollercoaster” phenomenon (77).

Even for those patients without comorbidities or illness requiring hospitalization, a large number of convalescent COVID-19 patients at four months post-infection are reported to have one or more residual organ system impairments as defined by quantitative magnetic resonance imaging (MRI) T1 mapping (12, 87). This phenomenon is termed Long COVID (or post-acute sequelae of COVID-19 [PASC]) and can involve any organ system (88). Hypercoagulability and VTE have been described as potential complications in Long COVID patients (88). In the convalescent COVID-19 patient, it is important to understand that the timing of surgery is a function of where the patient lies within the context of their individual immuno-thrombotic state (77).

Further research is necessary for determining potential biomarkers which may allow surgeons to weigh the risks and benefits of elective surgery. Multiple studies have shown persistently elevated D-dimer, fibrinogen, C-reactive protein (CRP), interleukin (IL)-4, IL-6, tumor necrosis factor (TNF)-α, interferon (IFN)-γ-induced protein 10, factor VIII, VWF, and plasma soluble thrombomodulin in patients up to six months post-recovery from COVID-19 (81, 89–94), indicating that these may serve as potential biomarkers for assessing the risk of postoperative complications. Hypercoagulability markers are often associated with postoperative complications in non-COVID-19 perioperative settings (e.g., PAI-1, TAFI, increased fibrinogen and platelet counts) (7, 95–97). Research on these and other biomarkers in assessing postoperative morbidity and mortality in convalescent COVID-19 patients undergoing elective surgery, however, is lacking. Future studies are required in order to determine the most prognostic biomarkers for evaluating this patient population (88).

COVID-19 and the subsequent damage to endothelial cells result in a progression from hemostasis to a relatively prothrombotic/ antifibrinolytic state (31, 38, 43–45). Clinical data demonstrate significant thrombophilia with fibrinolysis shutdown being a primary component, regulated by higher circulating levels of antifibrinolytic factors, namely PAI-1 and TAFI. Yet, coagulation is a rigorously regulated process: fibrinolytic and thrombotic pathways are continuously competing against each other such that neither hemorrhage nor thrombosis is favored under normal physiological conditions (98). Therapeutic strategies for COVID-19 patients that utilize these findings, including the use of fibrinolytics, have been under examination and show potential for improving patient outcomes. For patients being treated with COVID-19, therapeutic anticoagulation is the standard regimen for patients with macrothrombosis. Furthermore, the use of anticoagulant heparinoids is advised for all COVID-19 patients (99). The use of tPa has been suggested for patients with severe ARDS caused by COVID-19 (100). In these studies, the use has been late in the disease course. Theoretically, if tPa is used earlier during the hypercoagulable stages of the disease, the fibrinolytic and therapeutic effect may be greater than those reported in the recent literature. Also, when administered later in the course of the disease—as the cytokine storm recedes—the patients may be prone to hemorrhage similar to anticoagulated COVID-19 patients (17, 101).

Therapeutic anticoagulation and thromboprophylaxis for the hospitalized COVID-19 surgical patient vary substantially. Recommendations have been made from adherence to standard VTE prophylactic guidance to intermediate or therapeutic dosing for moderately ill COVID-19 patients (85, 86). The preferred agents have been enoxaparin with anti-Xa monitoring or unfractionated heparin with either activated partial thromboplastin time (aPTT) or anti-Xa guidance. This heterogeneity is based on large multiplatform randomized controlled trials (RCTs) as well as society consensus statements. Recent guidelines and consensus statements have considered conditional support for therapeutic and/or intermediate heparinoid thromboprophylaxis for moderately ill COVID-19 patients not requiring high-flow oxygen (Table 1) (24–26, 85, 86, 99, 102–104). The importance of this foundational literature has been highlighted by observations that clinicians find it difficult to practice medicine during the COVID-19 pandemic bereft of RCTs to guide treatment (105). Therefore, reliance on categorization of hemostatic phenotype by VHAs fulfills the criteria of personalized-based medicine as a guidance for anticoagulation and thromboprophylaxis for the COVID-19 surgical patient.

For elective cases, a high incidence of patients discharged from the hospital have VTEs within 90 days of discharge from COVID-19 (16). In addition, a subsection of the population who have COVID-19 and have undergone surgery have a markedly elevated rate of VTEs (9). Because of the absence of specific RCTs recommending postoperative DVT prophylaxis in this group of patients, use of Elective Surgery Acuity Scale (ESAS) guidelines as well as co-morbidities and adjunctive VHA analysis would allow for postoperative DVT prophylaxis similar to that which has been recommended for the post-COVID discharged patient. Specifically, the recommendations vary from 10 mg rivaroxaban for 35 days, 2.5 mg apixaban b.i.d. for 35 days, or for patients with normal renal function, 40 mg enoxaparin for 35 days (102, 106, 107). Specific co-morbid analysis using conventional coagulation tests with adjunctive TEG-guided anticoagulation for COVID-19 patients with and without macrothrombosis has demonstrated the ability of the TEG to assist in the prediction of bleeding and clotting in this group of patients (17, 108). Similarly, the large RCTs which have demonstrated therapeutic benefit of heparinoids in moderately ill COVID-19 patients would be refined by the addition of VHAs to guide anticoagulant therapy (17, 85, 86, 109).

As has been shown, so-called “intermediate” and therapeutic anticoagulation has been found to protect patients with moderately severe COVID-19 pneumonitis (86). Surgeons will find themselves during the acute and subacute period considering emergent and semi-emergent procedures for patients on anticoagulation not just for known macrothromboses but also for the specific antiviral and antiinflammatory functions of heparinoids in these patients (85, 86, 109). In addition to conventional coagulation tests, anticoagulation for these patients is facilitated by adjunctive hemostatic monitoring with VHAs (17, 20–22).

The sequelae of Long COVID may be a function of residual endothelial damage from the SARS-CoV-2 endothelial cell invasion (88, 110). As such, thromboprophylaxis for postoperative convalescent COVID-19 patients should draw from strategies to manage acute COVID-19 patients along with the strategies for non-COVID-19 patients undergoing elective surgery.

Surgeons—because of their more than half century experience with TEG/ROTEM to diagnose and treat coagulopathies in liver transplantation, cardiac surgery, and trauma—have been at the forefront of pathophysiologic investigations of CAC (111). Because of surgeons’ historical experience on the intricacies of hemostasis, surgeons have employed TEG/ROTEM to guide and personalize anticoagulation during the COVID-19 pandemic (20–22, 28, 29, 101, 112). TEG/ROTEM have also been used to profile postoperative patients at risk for VTE (23, 113–116). This background in using TEG/ROTEM to predict a patient’s fibrinolytic phenotype prepares the surgeon to manage CAC patients. Given the significant variation in risk of the development of either a hypocoagulopathic- or hypercoagulopathic-related complication in the perioperative period as a function of the severity of COVID-19 illness, it is difficult to rely on arbitrary standards regarding the timing of surgery and the nature of anticoagulation and thromboprophylaxis in this group of patients (17, 28, 29, 31, 108).

The recent evolution of the less virulent but more infectious variants, such as the omicron (B.1.1.529), may render guidelines regarding the timing and nature of therapeutic anticoagulation and thromboprophylaxis for the surgical patient less applicable. Although there is no data directly demonstrating lower risk of thrombosis in patients infected with omicron versus other more virulent variants, thrombosis risk in COVID-19 patients is in large part a function of illness severity (117, 118). By logical extension of this evidence, it is likely omicron infection carries less thrombotic risk compared to more virulent variants such as alpha or delta. Age, co-morbidities, and overall clinical picture are paramount to consider when deciding to what degree the individual patient should be anticoagulated. There are no plasma-based laboratory tests which allow for prediction of the likelihood of perioperative complications regarding coagulation for the surgical patient with either acute or remote COVID-19 infection. Historically, VHAs have been used to predict both bleeding and clotting in patients undergoing liver transplantation, cardiac surgery, trauma surgery, and most recently, bleeding and clotting obstetric patients. Most recently, adjunctive TEG has demonstrated prediction of VTE in critically ill COVID-19 patients (20–23). However, categorizing patients’ fibrinolytic and coagulopathic phenotype with TEG/ROTEM, as has been done by surgeons for decades, may allow the surgeon to better predict the development of perioperative clot and to manage pre- and post-surgical clots more effectively in the COVID-19 patient. In addition, platelet activation can be graded with plasma microclot density analysis, which has demonstrated that Long COVID patients have a persistent coagulopathy and increased microclot formation (119). Together, TEG/ROTEM with microclot analysis may predict the surgical patient’s position in the hemostatic and fibrinolysis spectrum in the absence of evidenced biomarkers. Figure 3 illustrates the ‘rollercoaster’ phenomenon of hospitalized COVID-19 patients as characterized by TEG/ROTEM in the acute and subacute periods, as well as the remote period after discharge (77). Figure 4 provides a prototype spectrum of CAC wherein the patient’s individual coagulopathy may be modified by the COVID-19 variant and is characterized by TEG/ROTEM and plasma microclot analysis. Studies are in progress regarding microclot analysis as an enhanced method of hemostatic grading (78).

Obstetricians have long experience with surgical interventions on patients who have peripartum coagulopathies wherein the patient may switch between hemorrhagic and thrombotic phenotypes rapidly. Obstetricians have similar experience as CAC with pathologies such as preeclampsia, Hemolysis, Elevated Liver enzymes, and Low Platelets (HELLP) syndrome, morbidly adherent placenta (MAP) and other significant diseases associated with the peripartum state (145–156). This spectrum of disorders in the peripartum patient allow pathophysiological comparison to the hemostatic derangement of CAC in the nonpregnant surgical patient (29, 157). In each disease entity, there is endotheliitis that results in an immuno-thrombotic crosstalk resulting in local thrombosis and/or hemorrhage at the level of the inflamed endothelium (17, 157). For example, prepartum patients with preeclampsia must be given thromboprophylaxis to prevent clotting, but during parturition, they are at higher risk for bleeding, and again return to a hypercoagulable state postpartum (157). In tandem, postpartum patients with preeclampsia or other underlying risk factors for a hypercoagulable state should be treated for at least six weeks with thromboprophylaxis postpartum (146). Hence, discussion of the obstetrical approaches to providing thromboprophylaxis serves as an ideal foundation for describing the other surgical disciplines with more straightforward pathophysiological proclivities for the formation of perioperative clots. International guidelines for thromboprophylaxis for women who have undergone a C-section are heterogeneous in their recommendations regarding the timing and duration of thromboprophylaxis (146, 158).

In the United States and other countries, thromboprophylaxis for women undergoing C-sections has been described by the American College of Obstetricians & Gynaecologists guidelines that recommend thromboprophylaxis for all patients with C-sections who have at least one major indication or two minor indications for anticoagulation (159). The three major indications are previous VTE, body mass index (BMI) > 35, and thrombophilia. The minor indications are preeclampsia, hypertension, diabetes, peripartum infection, and other comorbidities (145, 159–163). Since guidelines are dynamic, the inclusion of COVID-19 as a minor indication seems reasonable. However, it would also be judicious to refer to the spectrum of diseases whereby women with severe COVID-19 are included in the group of patients with major indications for anticoagulation such that they would receive six weeks thromboprophylaxis. This paradigm has been useful in the most recent literature and serves as a template for applications to the other disciplines.

Since there is sparse literature regarding the guidance of thromboprophylaxis and treatment of the peripartum COVID-19 patient, surgeons must rely on consensus recommendations from interim guidelines. These recommendations for peripartum anticoagulation and thromboprophylaxis have been extrapolated from the COVID-19 literature for non-pregnant patients. Interim guidelines have been published by many organizations with specific references to pregnant women (164–166).

Similar to obstetric patients, there is a spectrum of risk for developing postoperative VTE as a function of COVID-19 illness severity in patients undergoing orthopaedic surgery. Significant literature has demonstrated the benefit of serial VHAs to predict postoperative VTE (167–169). Therefore, for a disease which, by its very nature presents with a hypercoagulopathic state manifested clinically by increased VTEs and arterial thromboses, the use of VHAs in this COVID-19 population is a logical extension. While consensus recommendations have been proposed to optimize safety for patients undergoing elective surgery after previously being diagnosed with COVID-19, adjunctive VHAs may enhance these guidelines to better predict VTE and guide anticoagulant therapy postoperatively (131, 170–172).

Early intervention tends to be optimal for fracture fixation, but timing of surgery is historically complicated in patients with hemostatic derangement such as that which is induced in the post-COVID-19 patient. Decreased time between hip fracture and surgery correlates with decreased morbidity and mortality. However, correct timing of surgery in patients diagnosed with COVID-19 is difficult to assess (173). As an example of the heterogeneity of recommendations, it has been noted that a delay in fracture fixation of up to three months postinjury is acceptable, allowing for the risks of delayed surgery to be weighed against the risks of early fracture fixation performed during early post-COVID-19 prognosis (170).

Therefore, it is generally recommended that clinicians address each post-COVID-19 case individually and tailor a unique treatment plan for each patient based on their severity of injury and COVID-19 prognosis (172, 173). Patients waiting for elective orthopaedic surgery need to be reassessed in orthopaedic pathology, COVID-19 prognosis, surgical fitness, and desire to undergo the procedure with regards to evolving risks and benefits. Robust appraisal during the preoperative period to evaluate fitness for surgery is necessary to mitigate the risk of postoperative complications and decrease strain on postoperative intensive care units (170).

Specific orthopaedic society recommendations are outlined in Table 2. The American Association for Hand Surgery suggests delaying surgery based on the capacity to care for COVID-19 patients rather than postoperative prognosis (128). The American Orthopaedic Association offers broad suggestions regarding delay of surgery based on clinical need and institutional availability (130). Most of these orthopedic organizations do not have specific guidelines for delaying surgery to reduce the incidence of VTEs. However, the European Hip Society and European Knee Associates recommend delaying arthroplasty for six weeks following infection for otherwise healthy individuals, and for infected individuals with one or more comorbidities delaying the surgery for at least 8 weeks (131). When compared to anesthesia and non-orthopaedic society recommendations, the recommendations from European societies seem the most judicious provided the well-recognized increases in mortality and VTE complications associated with post-COVID-19 elective surgeries (13, 134). An example ESAS for delaying procedures is provided in Table 3.

The COVID-19 pandemic resulted in a significant reduction of general surgical procedures, including procedures for both benign and malignant diseases. While elective surgery for benign disease was intentionally halted during the pandemic, the reduction in procedures for malignancies was likely an unintentional consequence of reduced patient access to clinical examinations and diagnostic testing as a result of limited capacity of healthcare systems (174).

At the beginning of the pandemic, it was recommended that emergent cases be individualized based on patient risk, urgent cases be delayed at least until COVID-19 infection clears, and elective cases not be performed and potentially delayed for months (175). Emergency surgery was performed on patients regardless of their COVID-19 infection status.

The ACS and the American Society of General Surgeons initially published guidelines based on risk factors and patient benefits related to SARS-CoV-2 transmissibility during acute infection. These guidelines are heterogeneous and do not specifically address hemostatic complications related to elective and acute surgery during acute and convalescent COVID-19 (133, 134). These two associations adopted the CMS 3-tiered framework for urgency of procedures based on the ESAS (134, 136). This three-tiered system is defined by Tier 1, elective surgery which is to be postponed; Tier 2, intermediate acuity surgery postpone if possible; and Tier 3, indications for acute surgery where postponement is not an option (136). Table 4 specifically defines example surgical procedures based on this three-tiered system.

With regards to transplant surgery, COVID-19 infection following organ implantation is associated with increased mortality (176, 177). Pre-vaccination prior to transplant has been suggested to reduce the risk of mortality (178). In the context of receiving an organ from a COVID-19 positive donor, there is growing evidence that viral transmission from abdominal organs is a nearly negligible risk (179). This has led to a call for increased use of COVID-19 positive donors without evidence of systemic disease, as the low risk of transmission does not appear to outweigh the potential lifesaving benefit from organ transplantation (180). However, a positive PCR test in a recipient should delay the procedure, and a delay of at least two to four weeks of negative serologies is required for waitlist reactivation of immunosuppressed candidates after COVID-19 contraction.

The Society of American Gastrointestinal Endoscopic Surgeons has provided specific guidelines for gastrointestinal cancers similar to the ESAS (138). A large study of over four million cancer patients found that most oncological procedures can be delayed by four weeks without a significant impact on patient morbidity or mortality (181, 182). However, a patient’s age and comorbidities are critical for weighing the relative benefit and risk of potentially exposing the patient to COVID-19 as opposed to choosing alternative options. The resources available to the surgeon must also be considered, since the pandemic has caused large fluctuations in patient acuity, volume, and hospital resources (183). In COVID-19 positive patients with primary or secondary cancer, elective liver or adrenal resection should be delayed until patients fully recover from acute COVID-19. In cases of jaundice or infection, percutaneous transhepatic biliary drainage (PTBD) or endoscopic retrograde cholangiopancreatography (ERCP) should be first implemented as a bridge therapy (184).

The literature concerning timing of neurosurgical procedures has mostly considered SARS-CoV-2 transmissibility and healthcare worker safety (185–188). For example, it has been demonstrated that tracheostomies may be safely delayed two weeks, whereas craniectomy and tumor resections, as well as evacuation of subdural hematomas, need to be evaluated on a case-by-case basis (188, 189). Surgical treatment of chronic subdural hematoma, a usually successful intervention with a reported mortality rate of 3.7%, has a markedly increased mortality risk in COVID-19 positive surgical patients (190). Further investigation attributes multiple factors to this mortality rate, including thrombocytopenia, immune system impairment, and interstitial pneumonia progression post-surgery (191).

Like other surgical societies, there is heavy reliance on the modified ESAS for determining the timing of neurosurgical procedures for COVID (139). A similar 3-tiered system has been proposed regarding low, intermediate, and high acuity indications for neurosurgical intervention. Examples of surgeries that are divided into these three tiers are Tier 1, benign intracranial tumors which are low acuity; Tier 2, unruptured cerebral aneurysms and AV malformations as intermediate acuity; and Tier 3, malignant brain and spinal tumors for high acuity surgery where postponement is not an option (139). Table 2 and 5 summarizes current neurosurgical guidelines regarding the timing of surgery for COVID-19 patients.

Cardiothoracic and vascular surgery society guidelines have likewise adapted the CMS recommendations as well as ESAS guidelines for determining the timing of surgery during the COVID-19 pandemic (140, 141). The cardiothoracic guidelines have also benefited from the cardiology literature, which recommends adherence to standard anticoagulation procedures for patients with post-acute sequelae of COVID-19 who are undergoing percutaneous coronary intervention with or without angioplasty for ST segment elevation myocardial infarcts (192). During the acute period of COVID-19 infection, adherence to standard heparin boluses, anti-platelet, and intravenous and oral anti-factor agents is recommended without any change (193). For those patients whose intervention is complicated by a hypercoagulable state, treatment should be titrated with a personalized medicine approach and the use of VHAs to guide anticoagulation has been suggested (194–196). Acutely ill patients with severe coronary artery disease and valvular pathology not amenable to non-surgical interventions can either be operated immediately or temporized with a left ventricular assist device, intra-aortic balloon pump, or extracorporeal membrane oxygenation while waiting for the cytokine storm to abate if clinically possible (197). These guidelines are heterogeneous and likewise founded on the ASA and ACS three-tiered system of classifying patients with COVID-19 who require surgery (13, 134).

Provided the protracted nature of this pandemic, cardiac surgery programs must continue to proactively manage every patient on their waitlist with re-expansion of case volumes. Aspects of this management have been divided into three separate tiers of so-called ‘ramp up’ levels which determine the timing of surgery based on a combination of return to surgical case volume and acuity of indication for cardiothoracic surgery (141, 198).

The Canadian Cardiothoracic Society has described the following criteria: For ramp up phase one where the surgical volume is increased 0-25%, the patients who should avoid surgery when possible include frail elderly patients (clinical frailty score > 4) and vulnerable co-morbid patients including those with renal insufficiency, poor ejection fractions, and advanced congestive heart failure. Overall, in a phase one scenario, the cardiothoracic surgeon should attempt to avoid complex procedures including re-operative surgery while prioritizing CABG, isolated valve procedures, and less complex procedures to maximize patient flow. There should be an emphasis on patients with aortic stenosis and coronary artery disease with prognostic benefit, such as critical aortic stenosis and left main coronary disease. In the ramp up phase two, where surgical volume is increased 25-50%, inpatient urgent and emergency surgeries should be continued with broadening inclusion of appropriately prioritized outpatients. Ramp up phase three occurs with 50-100% increase in capacity with a return to normal outpatient services while continuing to prioritize those as greatest risk such as asymptomatic and severe mitral regurgitation, atrial septal defect or patent foramen ovale surgery, and asymptomatic aneurysm with demonstrated stable size.

In the thoracic surgery literature, a four-tier system of patient triage has been recommended by The Society of Thoracic Surgeons COVID-19 Task Force and the Workforce for Adult Cardiac and Vascular Surgery. For consistency here, we provide a three-tiered ESAS in Table 6.

Systemic anticoagulation with intravenous unfractionated heparin should be provided for all patients with acute limb ischemia (ALI). The performance of endovascular or open procedures for ALI is a function of the acuity of the limb ischemia and its relation to the hemostatic derangement present in the COVID-19 patient. There is no high-quality data to suggest that either open or vascular intervention is the preferred treatment ALI. It has been noted that a heparin resistance is in acute COVID-19 illness is common, while at the same time, the capricious nature of the cytokine storm causes the COVID-19 patient to have abnormal coagulation patterns. This interference with therapeutic anticoagulation requires frequent monitoring of not only aPTT and anti-Xa levels, but also with VHAs (17, 20–23, 108).

Similar guidelines based on the CMS and ESAS criteria have been adapted to the oculo/plastic and reconstructive procedures (199, 200). These guidelines are based on the three-tiered system which also incorporates the supply and demand for elective and acute surgeries and the acuity of the surgical intervention required. Of all specialties, the oculoplastic international societies have the most exhaustive list of procedures incorporated within the context of the three-tiered system since most of their surgeries are elective (201). These are summarized in Table 7 below.

Of particular importance for this group of patients is the viability of microvascular flaps which, because of the hypercoagulability mediated by the immuno-thrombotic derangements that are part of CAC, require evaluation by the surgeon for the timing of surgery and the risk of ischemic flap loss. For example, criteria for the administration of continuous unfractionated heparin have been suggested for microvascular free flaps after head and neck cancer excision (202, 203). Recent publications have demonstrated the use of VHAs in guiding anticoagulation therapy to maintain vascular patency of microvascular vessels in flap surgery and reconstruction (204).