A 74-year-old male patient was sent to Huangshi hospital of Traditional Chinese Medicine on January 31, 2020, with two days long of fever, cough, headache, diarrhea, vomiting, fatigue and dyspnea. Those characteristics, weakness in the right extremities, distortion of commissure and lalopathy had already emerged at middle January.
Blood tests revealed elevated monocyte counts (0.64 g/L, [normal, 0.10–0.60 g/L]), mean platelet volume (12.00 fL, [normal, 8.50–11.80 fL]) and percentage of monocyte (16.30%, [normal, 3.00–10.00%]), nevertheless eosinophil count (0.00 g/L, [normal, 0.02–0.52 g/L]), percentage of eosinophil (0.00%, [normal, 0.40-8.00%]), blood platelet count (87 g/L, [normal, 125–350 g/L]), mean corpuscular hemoglobin concentration (315 g/L, [normal, 316–354 g/L]) and hemoglobin concentration (129 g/L, [normal, 130–175 g/L]) lowered on February 3, 2020. Throat swab was taken to detect respiratory tract pathogens after blood testing and listed in Table 1. Coagulation profiles were tested and showed in Table 2. D-dimer and Fibrinogen degradation products increased a lot compared with normal reference range while other items were normal. As 80 kilometers away from COVID-19 outbreak site, Wuhan, SARS-Cov-2 RNA testing was unavailable in early February in Huangshi hospital of Traditional Chinese Medicine. We speculated that he got SARS-Cov-2 infected, then he was send to thoracic computed tomography (CT) diagnosis.
Table 1
Respiratory tract pathogens PCR detection.
Items | Results | Ref range |
Legionella pneumophila | Not detected (Negative) | Negative |
Mycoplasma pneumoniae | Not detected (Negative) | Negative |
Q hot rickettsia | Not detected (Negative) | Negative |
Chlamydia pneumoniae | Not detected (Negative) | Negative |
Adenoviridae | Not detected (Negative) | Negative |
Respiratory syncytial virus | Not detected (Negative) | Negative |
Influenza A virus | Not detected (Negative) | Negative |
Influenza B Virus | Not detected (Negative) | Negative |
Parainfluenza virus | Not detected (Negative) | Negative |
Table 2
Items | Results | Unit | Ref range |
prothrombin time | 11.60 | S | 9.00–14.00 |
International normalized ratio of prothrombin time | 0.91 | -- | 0.85–1.15 |
Activated partial thromboplastin time | 27.3 | S | 20.0–41.0 |
Thrombin time | 12.2 | S | 8.0–14.0 |
Fibrinogen | 3.98 | g/L | 2.00–4.00 |
D-dimer | 4.81 | µg/mL | 0-0.50 |
Fibrinogen degradation products | 143.25 | µg/L | 0–5.00 |
Thoracic CT scan showed ground-glass opacities in the right and left middle lobes, indicating the possibility of viral pneumonia on February 5, 2020 (Fig. 1). Based on the diagnosis, he was hospitalized for further investigation of suspected COVID-19. Based on the CT scanning results and clinical features, antiretroviral, antispasmodic and antiasthmatic expectorant therapy were given to the patient.
On February 7, thoracic CT scan showed aggravation of ground-glass opacities in both lobes (Fig. 2) compared to results on February 5. Blood tests On February 7 showed increased neutrophile granulocyte count and ratio which indicated pathogenic infection. On February 9, blood tests showed elevated WBC count, neutrophile granulocyte count and ratio, and monocyte count while percentage and count of eosinophil and lymphocyte lowered. Since lack of SARS-Cov-2 RNA testing products at that special time in Huangshi in early February, no nucleic acid results could provide diagnosis of COVID-19.
Coagulation profiles were tested on February 10, 14, 20, 24, 25, March 1, 2, 5, 10, 14 and 20, among the items D-dimer (Normal range, 0-0.50 µg/mL) all overstepped except March 20 (Fig. 3). Previous studies demonstrated that D-dimer levels were a vital indicator in predicting COVID-19 infection and in-hospital mortality[10]. In early stage of viral infection, D-dimer value was 4.81 µg/mL which increased a lot compared with normal range. We then investigated the prothrombin time (PT), thrombin time (TT) and fibrinogen (Fg) which were also significant indicators in confirmation of COVID-19 infection. PT and Fg elevated in the middle infection period, while TT increased in the early stage (Fig. 4).
In the middle of February, all of a sudden, the patient got right limb weakness accompanied with crooked mouth, speech barriers and other discomfort. Then the patient was sent to cranial CT detection on February 20 and 26, and cranial CT scan showed cerebral infarction in bilateral basal ganglia area, radial coronal area and bilateral frontal parietal lacunar, partial softening lesion formation and leukoencephalopathy and brain atrophy (Figs. 5 and 6). Anti-infection, anti-platelet aggregation and circulation improving treatment were given to the patient.
Through asking, we know the patient had a history of hypertension and type 2 diabetes. Physical examination showed blood pressure 135/80 mmHg, heart beats 80 times/min, body temperature 37℃, no yellowing in the whole skin, no lymph nodes enlargement in the superficial layer, clear respiratory sound in both lungs, no rales and dryness in both lungs, regular heart rhythm, no murmurs, flat and soft abdomen, and no swelling in both lower extremities. Three-dimensional reconstruction of the lungs, mediastinum, heart and ribs showed both lungs of viral infection, calcification of aorta and coronary artery wall, arteriosclerosis, increased and enlarged lymph nodes in the mediastinum and local adhesion of the pleura of both lungs, multiple local circular light-transmitting areas in the lower lobe of both lungs and emphysema with interstitial pneumonia on February 22. Compared with chest CT on February, the lesions in the upper lobe of left lung and the lower lobe of right lung expanded, while the lesions in the lower lobe of left lung and the upper lobe of right lung narrowed
SARS-Cov-2 antibodies were tested on March 1, II IgG, 123.64 AU/mL, II IgM 16.89 AU/mL, these indexes exceeded the normal range (0–10.00 AU/mL). On March 3, the patient was transferred to Huangshi Central Hospital for systemic detection and treatment. On March 5, both II IgG and II IgM were detected once more, IgG was 77.80 AU/mL which elevated a lot compared with norm, while II IgM gained 5.72 AU/mL which located at normal range. The positive of SARS-Cov-2 II IgG together with CT results confirmed the SARS-Cov-2 pneumonia.
On admission, the patient suffers from fever, cough, head pain and dyspnea, as of COVID-19 epidemic, we firstly used anti-viral therapy. As the physical condition was getting better, we tended to additional detection. Cerebral CT scan showed cerebral infarction and encephalatrophy symptoms on March 10, and the situation got worse on March 16. Pulmonary function test and evaluation showed delightful consequence and PCR confirmed SARS-Cov-2 negative on March 19. Body temperature was 36.5℃, and blood pressure was 120/75 mm Hg, with a respiratory of 19 breaths per minute and heart rate of 75 beats per minute. He had no cough, dyspnea t rest, chest distress and shortness of breath, chest pain, gasp and ventilator assistance. oxyhemoglobin saturation reached 100%.
Recommended medication guides were suggested as follows, for antiplatelet aggregation (Clopidogrel hydrogen shlfate tablet 25 mg po qd), for lowering blood lipid and stabilizing plaque (Rosuvastatin 5 mg po qd), for controlling heart rate and protecting heart muscle (Metoprolol tartrate controlled-release tablet 25 mg po qd), for controlling blood pressure (Felodipine sustained release tablet 5 mg po qd), for dissipating phlegm (Acetylcysteine Effervescent Tablets 0.6 g po bid), for antiviral infection (Imipenemastatin 0.5 g IV ) and accompanied with rehabilitation training therapy (PT OT therapy).
On March 21, the patient told brief palpitation, but vital signs were stable. Soon myo-cardial enzymonram were dectected, troponin (0.01 ng/mL) and B natriuretic sodium (50 pg/mL) both demonstrated normal. SARS-Cov-2 nucleic acid testing proved negative on March 31. The patient was physically stable and allowed discharged from hospital on April 3. In the following months, we kept on supervising the patient’s physical conditions regularly, and no obvious sequela showed.