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==Acute Respiratory Distress Syndrome==
=Cardiovascular Disorders and COVID-19=
* The novel coronavirus was named as the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) due to its high similarity to SARS-CoV, which caused acute respiratory distress syndrome (ARDS) in 2002–2003.
====In-hospital SCD====
* SARS-CoV-2 virus primarily affects the respiratory system causing wide variety of respiratory symptoms which can range from symptoms of lower respiratory tract infection to severe hypoxia to acute respiratory distress syndrome within a very short span of time.
=====Pathophysiology=====
 
*'''Drug induced:'''
===Epidemiology===
Since the [[COVID-19]] [[pandemic]], several [[pharmacological]] [[therapies]] have been proposed, one of them is of two [[anti-malarial]] and [[antirheumatic]] drugs called [[Chloroquine]] or [[Hydroxychloroquine]]. Due to their cost-effectiveness and easy availability, there is a surge in the use of [[Chloroquine]] and [[Hydroxychloroquine]], with or without [[Azithromycin]]. The [[clinical trials]] in order to estimate their [[efficacy]] are still in the preliminary stage, however, a notable concern is of their [[cardiac]] [[adverse effects]]. This includes [[QT prolongation]] and [[Torsade de pointes]] (TdP) leading to [[sudden cardiac death]]. The risk is there when these drugs are prescribed separately, however it increases several folds when these drugs are administered together, especially in patients with underlying [[hepatic]] [[disease]] or [[renal failure]].
* Incidence is higher in the elderly and much lower in children
*'''Genetic susceptibility:'''
* Higher mortality rate is seen in the elderly.
[[Epidemiological]] studies have shown that [[African Americans]] have higher [[COVID-19]] associated [[morbidity]] and [[mortality]] as compared to people from other ethnic groups. Recent studies show that this ethnic predilection is due to the genetics factors which contribute to a common ion channel variant p.Ser1103Tyr-SCN5A which confer an increased risk of drug-induced long QT syndrome (DI-LQTS) and drug-induced sudden cardiac death (DI-SCD). p.Ser1103Tyr-SCN5A generates late or persistent sodium current which is further aggravated by [[hypoxia]] or [[respiratory acidosis]] secondary to [[lungs]] involvement in [[COVID-19]]. This has and has been linked to an increased risk of ventricular arrhythmia (VA) such as torsade de pointes  and sudden cardiac death (SCD) in African Americans.
 
===Pathophysiology===
 
* ARDS arises as a complication of COVID-19 infection due to acute inflammation of the alveolar space which prevents normal gas exchange. The increase in proinflammatory cytokines within the lung leads to recruitment of leukocytes, further propagating the local inflammatory response
* The cytokine storm results with a violent attack by the immune system to the body, which causes acute respiratory distress syndrome. [13].  
* The cytokine storm and the deadly uncontrolled systemic inflammatory response resulting from the release of large amounts of proinflammatory cytokines (IFN-a, IFN-g, IL-1b, IL-6, IL-12, IL-18, IL-33, TNF-a, TGFb, etc.) and chemokines (CCL2, CCL3, CCL5, CXCL8, CXCL9, CXCL10, etc.) by immune effector cells ends with ARDS in SARS-CoV infection [14].  
*Patients show  elevated levels of IL-6, IFN-a, and CCL5, CXCL8, CXCL-10 in serum compared to those with the mild-moderate disease [11]
* This results in acute inflammation within the alveolar space and prevention of normal gas exchange.
*Patients infected with COVID‐19 exhibit coagulation abnormalities.<ref name="pmidPMID: 32302448">{{cite journal| author=Ranucci M, Ballotta A, Di Dedda U, Bayshnikova E, Dei Poli M, Resta M | display-authors=etal| title=The procoagulant pattern of patients with COVID-19 acute respiratory distress syndrome. | journal=J Thromb Haemost | year= 2020 | volume=  | issue=  | pages=  | pmid=PMID: 32302448 | doi=10.1111/jth.14854 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32302448  }} </ref> This procoagulant pattern can lead to acute respiratory distress syndrome.


===Diagnosis===
====Out of hospital Sudden cardiac arrest and death====
====Laboratory findings====
====Epidemiology====
* Blood plasma has elevated levels of IL-6, IL-1, tumor necrosis factor-α (TNF α) and C-reactive protein.
* Mild thrombocytopenia
* Increased D-dimer levels. The elevated level of D-dimer is strongly associated with a higher mortality rate.
* Increased fibrin degradation products
* Increased fibrinogen.
* Prothrombin time and activated partial thromboplastin time may be slightly elevated.


====Imaging studies====
*'''Incidence'''
* Chest CT scan shows characteristic ground-glass opacities (GCO). This indicates the presence of exudate in the bronchoalveolar airspace.
:*There is a two-times rise in the [[incidence]] of Out of hospital [[Sudden cardiac arrest]] (OHCA) during the [[COVID-19]] [[pandemic]] as compared to the non-pandemic time period.<ref name="pmidPMID: 32473113">{{cite journal| author=Marijon E, Karam N, Jost D, Perrot D, Frattini B, Derkenne C | display-authors=etal| title=Out-of-hospital cardiac arrest during the COVID-19 pandemic in Paris, France: a population-based, observational study. | journal=Lancet Public Health | year= 2020 | volume= | issue= | pages=  | pmid=PMID: 32473113 | doi=10.1016/S2468-2667(20)30117-1 | pmc=7255168 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32473113  }} </ref>
* Lung biopsy shows fibrin deposition.


===Signs and Symptoms===
*'''Mortality'''
:* [[Dyspnea]]: The onset of [[dyspnea]] is relatively late around the 6th day.<ref name="pmidPMID: 32105632">{{cite journal| author=Yang X, Yu Y, Xu J, Shu H, Xia J, Liu H | display-authors=etal| title=Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. | journal=Lancet Respir Med | year= 2020 | volume= 8 | issue= 5 | pages= 475-481 | pmid=PMID: 32105632 | doi=10.1016/S2213-2600(20)30079-5 | pmc=7102538 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32105632 }} </ref> <ref name="pmidPMID 32031570">{{cite journal| author=Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J | display-authors=etal| title=Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. | journal=JAMA | year= 2020 | volume=  | issue=  | pages=  | pmid=PMID 32031570 | doi=10.1001/jama.2020.1585 | pmc=7042881 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32031570  }} </ref>
There is a significant increase in the [[mortality rate]] of the OHCA [[patients]].<ref name="pmidPMID: 32473113">{{cite journal| author=Marijon E, Karam N, Jost D, Perrot D, Frattini B, Derkenne C | display-authors=etal| title=Out-of-hospital cardiac arrest during the COVID-19 pandemic in Paris, France: a population-based, observational study. | journal=Lancet Public Health | year= 2020 | volume= | issue= | pages= | pmid=PMID: 32473113 | doi=10.1016/S2468-2667(20)30117-1 | pmc=7255168 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32473113 }} </ref>
:*[[Acute]] [[Hypoxemia]] due to respiratory failure is a dominant finding.
:*[[Hypercapnea]] could be present but it is rare.


===Treatment===
*'''Age'''
==== Fluid and electrolytes management ====
Mean [[age]] 69·7 years is observed among patients who experienced Out of hospital [[Sudden cardiac arrest]] (OHCA) .<ref name="pmidPMID: 32473113">{{cite journal| author=Marijon E, Karam N, Jost D, Perrot D, Frattini B, Derkenne C | display-authors=etal| title=Out-of-hospital cardiac arrest during the COVID-19 pandemic in Paris, France: a population-based, observational study. | journal=Lancet Public Health | year= 2020 | volume= | issue= | pages= | pmid=PMID: 32473113 | doi=10.1016/S2468-2667(20)30117-1 | pmc=7255168 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32473113  }} </ref> .


==== Glucocorticoids ====
*'''Gender'''
Studies show that [[males]] have a slightly higher [[incidence]] of Out of hospital Sudden cardiac arrest (OHCA) as compared to the [[females]].<ref name="pmidPMID: 32473113">{{cite journal| author=Marijon E, Karam N, Jost D, Perrot D, Frattini B, Derkenne C | display-authors=etal| title=Out-of-hospital cardiac arrest during the COVID-19 pandemic in Paris, France: a population-based, observational study. | journal=Lancet Public Health | year= 2020 | volume= | issue= | pages=  | pmid=PMID: 32473113 | doi=10.1016/S2468-2667(20)30117-1 | pmc=7255168 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32473113  }} </ref>
*'''Race'''
A higher incidence is seen among Blacks as compared to whites.<ref name="pmidPMID: 32558876">{{cite journal| author=Lai PH, Lancet EA, Weiden MD, Webber MP, Zeig-Owens R, Hall CB | display-authors=etal| title=Characteristics Associated With Out-of-Hospital Cardiac Arrests and Resuscitations During the Novel Coronavirus Disease 2019 Pandemic in New York City. | journal=JAMA Cardiol | year= 2020 | volume=  | issue=  | pages=  | pmid=PMID: 32558876 | doi=10.1001/jamacardio.2020.2488 | pmc=7305567 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32558876  }} </ref>


====Mechanical Ventilation====
=====Pathophysiology=====
* Majority of COVID-19 patients with ARDS require mechanical ventilation for two weeks or more. The aim is to maintain oxygen saturation between 90 and 96%. The severe hypoxemia of the COVID-19 ARDS best responds when Positive end-expiratory pressure (PEEP) is high with Pplat ≤30 cm H2O. It is beneficial if the physician starts with higher than usual levels o PEEP (10 to 15 cm H2O).
*


==== Anticoagulant or thrombolytic therapy ====
=====Diagnosis====
* Fibrinolytic drugs such as tissue-type plasminogen activator (tPA) degrade pre-existing fibrin in the lungs.
*'''EKG'''
* Nebulizer plasminogen activators may provide more targeted therapy to degrade fibrin and improving oxygenation in critically ill patients. It is in Phase II of the clinical trial.
* Pulseless electrical activity


===Prevention===
=====Treatment=====
* The ARDS patients have an increased risk of hospital-associated venous thromboembolism (VTE). Due to this reason, it is advised to take low molecular weight heparin (LMWH) prophylactically in patients who do not have the contraindications. Studies have shown that the heparin, either unfractionated or LMWH, can also reduce inflammatory biomarkers hence could help in reducing the inflammation.
*'''Cardiopulmonary resuscitation'''
*
:*Immediate basic life support or advanced cardiac life support with an automatic external defibrillator is essential to safe the life of the patient. If the COVID-19 infection was confirmed, the EMS personnel is instructed to wear personal protective equipment (PPE) before performing cardiopulmonary resuscitation.https://costr.ilcor.org/document/covid-19-infection-risk-to-rescuers-from-patients-in-cardiac-arrest.
 
*'''Implantable Cardioverter Defibrillator (ICD)'''
=Cardiovascular Disorders and COVID-19=
:*An implantable cardioverter-defibrillator (ICD) is the preferred therapeutic modality in most survivors of SCA. This device does not prevent the recurrence of arrhythmia, instead, it terminates them  in case if they do recur.
*'''Pharmacologic therapy in survivors of sudden cardiac arrest'''
:*'''Antiarrhythmic drugs:'''Amiodarone is the most effective for preventing recurrent ventricular tachyarrhythmias, It is recommended to immediately give Amiodarone following an event of sudden cardiac arrest in patients with recurrent ventricular tachyarrhythmias as well as for those who have refused Implantable Cardioverter Defibrillator(ICD).
:*'''Beta blocker:'''It is recommended that almost all patients who survive an episode of sudden cardiac arrest should receive a beta-blocker as part of their therapy in combination with an antiarrhythmic drug, particularly in those patients who have survived sudden cardiac death due to ventricular tachycardia or ventricular fibrillation. Beta-blockers has shown to reduce the future incidence of sudden death.


=====Prevention=====
*Identification and treatment of acute reversible causes.
*Evaluation and management of structural heart disease and arrhythmia.


==Spontaneous coronary dissection==
==Spontaneous coronary dissection==

Latest revision as of 00:19, 25 June 2020

Cardiovascular Disorders and COVID-19

In-hospital SCD

Pathophysiology
  • Drug induced:

Since the COVID-19 pandemic, several pharmacological therapies have been proposed, one of them is of two anti-malarial and antirheumatic drugs called Chloroquine or Hydroxychloroquine. Due to their cost-effectiveness and easy availability, there is a surge in the use of Chloroquine and Hydroxychloroquine, with or without Azithromycin. The clinical trials in order to estimate their efficacy are still in the preliminary stage, however, a notable concern is of their cardiac adverse effects. This includes QT prolongation and Torsade de pointes (TdP) leading to sudden cardiac death. The risk is there when these drugs are prescribed separately, however it increases several folds when these drugs are administered together, especially in patients with underlying hepatic disease or renal failure.

  • Genetic susceptibility:

Epidemiological studies have shown that African Americans have higher COVID-19 associated morbidity and mortality as compared to people from other ethnic groups. Recent studies show that this ethnic predilection is due to the genetics factors which contribute to a common ion channel variant p.Ser1103Tyr-SCN5A which confer an increased risk of drug-induced long QT syndrome (DI-LQTS) and drug-induced sudden cardiac death (DI-SCD). p.Ser1103Tyr-SCN5A generates late or persistent sodium current which is further aggravated by hypoxia or respiratory acidosis secondary to lungs involvement in COVID-19. This has and has been linked to an increased risk of ventricular arrhythmia (VA) such as torsade de pointes and sudden cardiac death (SCD) in African Americans.

Out of hospital Sudden cardiac arrest and death

Epidemiology

  • Incidence
  • Mortality

There is a significant increase in the mortality rate of the OHCA patients.[1]

  • Age

Mean age 69·7 years is observed among patients who experienced Out of hospital Sudden cardiac arrest (OHCA) .[1] .

  • Gender

Studies show that males have a slightly higher incidence of Out of hospital Sudden cardiac arrest (OHCA) as compared to the females.[1]

  • Race

A higher incidence is seen among Blacks as compared to whites.[2]

Pathophysiology

=Diagnosis

  • EKG
  • Pulseless electrical activity
Treatment
  • Cardiopulmonary resuscitation
  • Implantable Cardioverter Defibrillator (ICD)
  • An implantable cardioverter-defibrillator (ICD) is the preferred therapeutic modality in most survivors of SCA. This device does not prevent the recurrence of arrhythmia, instead, it terminates them in case if they do recur.
  • Pharmacologic therapy in survivors of sudden cardiac arrest
  • Antiarrhythmic drugs:Amiodarone is the most effective for preventing recurrent ventricular tachyarrhythmias, It is recommended to immediately give Amiodarone following an event of sudden cardiac arrest in patients with recurrent ventricular tachyarrhythmias as well as for those who have refused Implantable Cardioverter Defibrillator(ICD).
  • Beta blocker:It is recommended that almost all patients who survive an episode of sudden cardiac arrest should receive a beta-blocker as part of their therapy in combination with an antiarrhythmic drug, particularly in those patients who have survived sudden cardiac death due to ventricular tachycardia or ventricular fibrillation. Beta-blockers has shown to reduce the future incidence of sudden death.
Prevention
  • Identification and treatment of acute reversible causes.
  • Evaluation and management of structural heart disease and arrhythmia.

Spontaneous coronary dissection

Pathophysiology In patients with an inflammatory overload, a localized inflammation of the coronary adventitia and periadventitial fat can occur. This could lead to the development of sudden coronary artery dissection in a susceptible patient. Signs and symptoms Treatment




 
 
 
 
 
 
 
Neurofibromatosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Neurofibromatosis 1
 
 
 
 
 
Neurofibromatosis 2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
NF1 tumor suppresor gene Mutation located on chromosome 17, encodes for neurofibromin
 
 
 
 
 
NF2 tumor suppresor gene Mutation located on chromosome 22, encodes for merlin
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
clinical features: Cafe-au-lait spots, multiple neurofibromas and lisch nodules
 
 
 
 
 
Clinical features: bilateral acoustic neuromas
 
 
 

Features of Wenicke-Korsakoff Syndrome
Associated conditions
  • Chronic alcoholism (most common).
  • Malnutrition.
Pathophysiology Thiamine deficiency impairs ATP generation leading to neuronal dysfunction and death. It mostly has paraventricular lesions involving mammillary bodies and dorsomedial bodies.
Clinical findings
  • Confusion.
  • Oculomotor dysfunction (horizontal nystagmus and bilateral abducens palsy)
  • Postural and gait ataxia.
  • Memory impairment (permanent).
Treatment
  • Intravenous thiamine.
  • Administration of glucose before the thiamine can worsen the symptoms.
Acne vulgaris
Clinical features
  • Comedonal acne:Closed or open comedones on forehead, nose and chin.
  • Inflammatory acne: Small, erythematous papules and pustules.
  • Nodular acne: Large painful nodules; sinus tracts and scarring.
Pathogenesis
  • Hyperkeratinization and obstruction of the pilosebacous follicles.
  • Sebaceous gland enlargement and increased sebum production.
  • Metabolism of sebaceous lipids by Cutibacterium acnes and release of inflammatory fatty acid.
  • Follicular inflammation and rupture,
Risk factors i) Increased circulating androgen (e.g. PCOS, puberty)

ii) Mechanical trauma/friction (excessive scrubbing, tight clothing)

iii) Comedogenic oil based skin and hair products.

iv) Excessive heat.

v) Obesity


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Criteria for the diagnosis of SLE
Clinical features Characteristics
1)Malar rash Fixed erythema, flat or raised, sparing the nasolabial folds
2)Discoid rash Erythematous raised patches with adherent keratotic scarring and follicular plugging.
3)Photosensitivity Rash due to unusual reaction to sunlight.
4)Oral ulcer Oral or nasopharyngeal ulcers, which may be painless.
5)Arthritis Non-erosive arthritis, involving >2 peripheral joints.
6)Serositis Pleuritis or pericarditis
7)Renal disorder Persistent proteinura ( >0.5g/24hrs) or cellular casts (red cell, granular or tubular).
8)Neurological disorder Seizure or psychosis, in the absence of provoking drugs or metabolic derangement.
9)Hematological disorder Haemolytic anemia or leucopenia (<4 x109) or lymphopenia (<1x109) or thrombocytopenia (<100x109) in the absence of offending drugs.
10)Immunological Abnormal titre of Anti-DNA antibodies or presence of Sm antigen or positive antiphospholipid antibodies.
11)Anti-nuclear Antibody (ANA) Abnormal ANA titre measured by immunofluorescence
Diagnosis of SLE is made in an adult if 4 out of 11 features are present either serially or simultaneously.
  • Erythematous raised patches with adherent keratotic scarring and follicular plugging.
 
 
 
 
 
 
 
Congenital anomalies of the urinary system
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Kidneys
 
Renal pelvis
 
Ureter
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Renal agenesis
 
Duplication of renal pelvis
 
Duplication of ureter
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Renal ectopia
 
 
 
 
 
Congenital megaureter
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Horseshoe kidney
 
 
 
 
 
Post-caval ureter
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Unilateral fusion
 
 
 
 
 
Ureterocele
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Congenital cystic kidney
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Infantile polycystic kidney
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Unlilateral Multicystic Kidney
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Simple cyst of the kidney
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Aberrant renal vessels
 
 
 
 
 
 
 
 
 







T
 
 
 
 
 
 
 
 
 
Mycosis fungoides
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stage IA-IIA
 
Stage IIA
 
 
Stage III
 
 
Stage IV
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

• Expectane policy
• Topical steroides [IV-A]
• nb-UVB[III,A]
• PUVA [III-A]
• Topical mechlorethamine [II,B]
• Local RT [IV,A]
 

• Skin direct therapy(SDT) + local radiotherapy
• ST[III+A]
• (SDT+) retiods[III,B]
• (SDT+) IFN a {III,B]
• TSEBT [III,A]
 
 

• (SDT+) retinoides
• (SDT+) IFNa
• ECPI INFa +/- rtinoides
• Low dose MTX
• [IV-B]
 
 

• Gemcitabine
• Liposomal doxorubicin
• Brentuximab vedotin[II,B]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

• (SDT+) retinoides [III,B]
• (SDT+) IFNa [III,B]
• Retinoides +IFN a [II,B]
• TSEBT [IV,A]
 

• Gemcitabin [IV,B]
• Liposomal doxorubicin [IV,B]
• Brentuximabvedotin [II,B]
• Combinatio Cht [Iv,B]
• AlloSCT[V,C]
 
 
TSEBT[LV,B]
 
 

• Combination Cht [IV,B]
• AlloSCT [V,C]
 
 
 
 
  1. ↑ 1.0 1.1 1.2 1.3 Marijon E, Karam N, Jost D, Perrot D, Frattini B, Derkenne C; et al. (2020). "Out-of-hospital cardiac arrest during the COVID-19 pandemic in Paris, France: a population-based, observational study". Lancet Public Health. doi:10.1016/S2468-2667(20)30117-1. PMC 7255168 Check |pmc= value (help). PMID 32473113 PMID: 32473113 Check |pmid= value (help).
  2. ↑ Lai PH, Lancet EA, Weiden MD, Webber MP, Zeig-Owens R, Hall CB; et al. (2020). "Characteristics Associated With Out-of-Hospital Cardiac Arrests and Resuscitations During the Novel Coronavirus Disease 2019 Pandemic in New York City". JAMA Cardiol. doi:10.1001/jamacardio.2020.2488. PMC 7305567 Check |pmc= value (help). PMID 32558876 PMID: 32558876 Check |pmid= value (help).
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