Epidemic Information

Diagnosis and Treatment Protocol for COVID-19 (Revised Trial Version 8)

• I. Etiological Characteristics

  The novel coronavirus (2019-nCoV) belongs to the β genus of coronaviruses, with an envelope and spherical/ovoid particles measuring 60–140nm in diameter. It contains five essential genes encoding four structural proteins—nucleocapsid protein (N), envelope protein (E), membrane protein (M), spike protein (S)—and RNA-dependent RNA polymerase (RdRp). The nucleocapsid
  is surrounded by the viral envelope (E protein), which embeds M and S proteins. The spike protein (S) facilitates cellular entry by binding to angiotensin-converting enzyme 2 (ACE-2). In vitro, the virus can be detected in human respiratory epithelial cells within ~96 hours, and in Vero E6 or Huh-7 cell lines after 4–6 days of culture.
  
  
  Coronaviruses are sensitive to ultraviolet light and heat. They can be effectively inactivated by 56°C for 30 minutes, ether, 75% ethanol, chlorine-containing disinfectants, peracetic acid, and chloroform (lipid solvents). Chlorhexidine does not inactivate the virus.

  II. Epidemiological Characteristics

  (1) Source of Infection

  Primary sources are COVID-19 patients and asymptomatic carriers, who are infectious during the incubation period and most contagious within 5 days of symptom onset.

  (2) Transmission Routes

  • Primary routes: Respiratory droplets and close contact.
  • Possible routes: Contact with virus-contaminated objects; aerosol transmission in relatively enclosed environments with prolonged exposure to high-concentration aerosols.
  • Indirect routes: Fecal-oral or aerosol transmission via environmental contamination (virus isolated from feces/urine).

  (3) Susceptibility

  Universal susceptibility. Infection or vaccination confers some immunity, but duration remains unclear.

  III. Pathological Changes

  (1) Lung

  • Gross findings: Patchy consolidation with diffuse alveolar damage and exudative alveolitis, featuring mixed acute and organizing lesions.
  • Microscopic findings
  • Electron microscopy: Coronavirus particles in bronchial epithelial/Type II alveolar cells.
  • Immunohistochemistry: Positive viral antigen/nucleic acid in bronchial/alveolar epithelial cells and macrophages.

  (2) Spleen, Hilar Lymph Nodes, and Bone Marrow

  • Spleen atrophy with reduced lymphocytes in white pulp; red pulp congestion and macrophage hyperplasia.
  • Lymph nodes show lymphocyte depletion and necrosis; positive viral nucleic acid in macrophages.
  • Bone marrow: Variable hematopoiesis, occasional hemophagocytosis.

  (3) Heart and Blood Vessels

  • Focal myocardial cell degeneration/necrosis; interstitial edema with mononuclear/lymphocyte infiltration.
  • Systemic small vessel endothelial damage, thrombosis, and infarction; hyaline thrombi in microvasculature.

  (4) Liver and Gallbladder

  • Hepatocyte degeneration/focal necrosis with neutrophil infiltration; sinusoidal congestion and portal lymphocytic infiltration.
  • Positive viral nucleic acid in liver/gallbladder.

  (5) Kidney

  • Glomerular capillary congestion; proteinaceous exudate in Bowman’s space.
  • Proximal tubular epithelial damage; distal tubular casts; renal interstitial congestion and microthrombi.

  (6) Other Organs

  • Brain: Edema, neuronal degeneration, and perivascular lymphocytic infiltration.
  • Adrenal glands: Focal necrosis.
  • Gastrointestinal tract: Mucosal epithelial damage and inflammatory infiltration.
  • Testes: Reduced spermatocytes and degenerative Sertoli/Leydig cells.
  • Viral detection in nasopharyngeal/gastrointestinal mucosa, testes, and salivary glands.

  IV. Clinical Features

  (1) Clinical Manifestations

  • Incubation period: 1–14 days (typically 3–7 days).
  • Common symptoms: Fever, dry cough, fatigue; some present with olfactory/gustatory dysfunction as the first symptom.
  • Severe cases: Dyspnea/hypoxemia after 1 week, progressing to ARDS, septic shock, metabolic acidosis, coagulopathy, and multi-organ failure.
  • Mild/asymptomatic cases: Low-grade fever, fatigue, or no symptoms; no pneumonia on imaging.
  • High-risk groups: Elderly, individuals with comorbidities, pregnant/postpartum women, and obese patients.
  • Pediatric cases: Mild symptoms or atypical presentations (e.g., gastrointestinal symptoms); rare multisystem inflammatory syndrome (MIS-C) in convalescence.

  (2) Laboratory Tests

  1. Routine tests
  1. Etiological/serological tests:
     • Nucleic acid testing: RT-PCR/NGS positive in respiratory, blood, fecal, or urine specimens (lower respiratory samples more accurate).
     • Serological testing: IgM/IgG positivity (low sensitivity in first week); prone to false positives; used for suspected cases with negative PCR or convalescent patients.

  (3) Chest Imaging

  • Early: Multiple small patchy shadows and interstitial changes (peripheral lung).
  • Progression: Bilateral ground-glass opacities/infiltrates; rare pleural effusion.
  • MIS-C: Cardiomegaly and pulmonary edema in patients with heart failure.

  V. Diagnostic Criteria

  (1) Suspected Case

  • With epidemiological history (any 1 item) + clinical features (any 2 items):
    1. Travel/residence in an affected community within 14 days.
    2. Contact with confirmed/asymptomatic cases within 14 days.
    3. Contact with febrile/respiratory symptom patients from affected communities within 14 days.
    4. Cluster incidence (≥2 cases with fever/respiratory symptoms in a small group within 2 weeks).
  • Without epidemiological history: Clinical features (any 2 items + positive IgM) or 3 clinical features.

  (2) Confirmed Case

  Suspected case + one of:
  
  
  1. Positive RT-PCR for SARS-CoV-2.
  2. Virus genome sequencing highly homologous to known SARS-CoV-2.
  3. Positive IgM/IgG antibodies.
  4. Seroconversion of IgG or ≥4-fold increase in convalescent IgG titer.

  VI. Clinical Classification

  1. Mild: Mild symptoms, no pneumonia on imaging.
  2. Moderate: Fever/respiratory symptoms with pulmonary imaging changes.
  3. Severe (adults):
     • RR ≥30 breaths/min; SpO2 ≤93% on room air; PaO2/FiO2 ≤300 mmHg; ≥50% lung lesion progression in 48 hours.
  4. Critical: Respiratory failure requiring mechanical ventilation; shock; multi-organ failure.

  VII. High-Risk Groups for Severe/Critical Illness

  • Age >65 years; comorbidities (cardiovascular disease, COPD, diabetes, cancer, etc.); immunocompromised status; obesity (BMI ≥30); late pregnancy/postpartum; heavy smokers.

  VIII. Early Warning Signs for Severe/Critical Illness

  • Progressive hypoxemia; rising lactate/inflammatory markers (IL-6, ferritin); lymphopenia; coagulation dysfunction; rapid lung lesion progression.

  IX. Differential Diagnosis

  • Other viral/bacterial respiratory infections (e.g., influenza, adenovirus, mycoplasma).
  • Non-infectious diseases (vasculitis, dermatomyositis, organizing pneumonia).
  • Pediatric cases: Kawasaki disease (with rash/mucosal lesions).

  X. Case Detection and Reporting

  • Suspected cases: Isolated in single rooms; nucleic acid testing within 2 hours; network reporting within 2 hours.
  • Exclusion of suspected cases: Two negative PCR tests (≥24-hour interval) and negative IgM/IgG 7 days after symptom onset.
  • Confirmed cases: Network reporting within 2 hours of diagnosis.

  XI. Treatment

  (1) Isolation and Care Setting

  • Suspected/confirmed cases: Isolated in designated hospitals; confirmed cases may share rooms; critical cases in ICU.

  (2) Supportive Care

  • Rest, hydration, oxygen therapy (nasal cannula, high-flow nasal cannula, noninvasive ventilation).
  • Avoid unnecessary antibiotics; monitor vital signs, labs, and imaging.

  (3) Antiviral Therapy

  Recommended agents (early use in high-risk patients)

  • Not recommended: Lopinavir-ritonavir/ribavirin alone; hydroxychloroquine/azithromycin.

  (4) Immunotherapy

  • Convalescent plasma: For severe/critical cases.
  • IV COVID-19 immunoglobulin: 20–40ml iv for moderate/severe cases.
  • Tocilizumab: 4–8mg/kg iv (max 800mg) for IL-6 elevated patients (≤2 doses).

  (5) Glucocorticoids

  Short-course use (3–5 days, ≤10 days) for patients with progressive hypoxemia/inflammatory storm (e.g., methylprednisolone 0.5–1mg/kg/day).

  XII. Discharge Criteria

  1. Afebrile for ≥3 days.
  2. Improved respiratory symptoms.
  3. Lung imaging shows resolving infiltrates.
  4. Two negative respiratory PCR tests (≥24-hour interval).

  XIII. Post-Discharge Management

  • 14-day home isolation and health monitoring; follow-up at 2 and 4 weeks.

  
  

  This protocol integrates China’s clinical experience and international guidelines to optimize COVID-19 management, emphasizing early detection, stratified care, and integrated Chinese-Western medicine approaches.

  
  

  Source: National Health Commission of China, Diagnosis and Treatment Protocol for COVID-19 (Revised Trial Version 8).

  
  

  
  

  
  

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