Table 1.
Parameter | Value |
---|---|
Sex: male/female ratio | 17:4 |
Age (years), mean (range) | 76 (53–96) |
Days in hospital (range) | 5.7 (0–16) |
Number (%) of intubated patients | 6 (30) |
Hours between death and autopsy (range) | 33.2 (11.0–84.5) |
Comorbidities, n (%) | |
Hypertension | 21 (100) |
Cardiovascular disease | 15 (71) |
Smoker | 8 (40) |
Pre‐obesity/obesity (WHO grade 1/2/3) | 10/1/1/4 (48/5/5/19) |
Diabetes mellitus | 7 (35) |
Chronic neurological condition | 5 (24) |
Chronic obstructive pulmonary disease | 3 (15) |
Malignancy | 3 (15) |
Chronic liver disease | 2 (10) |
Chronic kidney disease | 4 (19) |
Acquired immunosuppression | 1 (5) |
Initial clinical presentation, n (%) | |
Cough | 16 (76) |
Fever | 12 (57) |
Dyspnoea/tachypnoea | 10 (48) |
Pancytopenia | 2 (10) |
Diarrhoea | 1 (5) |
Acute or acute‐on‐chronic kidney injury | 12/18 (67) |
Radiological findings, n (%) | |
Ground glass infiltrates | 12 (57) |
Initial laboratory findings upon admission* | |
Haemoglobin (120–180 g/l), level (range) | 122.4 (97–209) |
Anaemia, n (%) | 7/11 (64) |
Total white blood cell count (3.5–10 × 10–9/l), value (range) | 8.7 (3.3–24.7) |
Leucopoenia, n (%) | 3/11 (27) |
Leucocytosis, n (%) | 3/11 (27) |
Neutrophils (40–74%), % (range) | 84 (63.4–96.4) |
Lymphocytes (19–48%), % (range) | 9.4 (1.0–23.5) |
Platelets (150–450 × 10–9/l), value (range) | 229.4 (25–433) |
Creatinine (μmol/l), level (range) | 254.7 (39–623) |
ASAT (11–34 U/l) (in 10 patients), level (range) | 67.2 (22–214) |
LDH (<135 U/l) (in 10 patients), level (range) | 450.5 (171–661) |
D‐dimers (<0.19 μg/ml) (in 5 patients), level (range) | 4.0 (0.4–10.4) |
IL‐6 (<7 ng/l) (in 5 patients), level (range) | 217.6 (103–278) |
Intake of agents interfering with RAAS † , n (%) | 14/21 (67) |
Intake of anticoagulation * , ‡ , n (%) | 11/11 (100) |
ASAT, aspartate aminotransferase; IL, interleukin; LDH, lactate dehydrogenase; RAAS, renin–angiotensin–aldosterone system; WHO, World Health Organization.
All normal ranges of laboratory values with designated units are shown in parentheses.
Basel cohort only.
Agents interfering directly or indirectly with the RAAS: angiotensin‐converting enzyme inhibitors, angiotensin II receptor blockers, and aldosterone inhibitors.
Agents included heparin and its derivatives, new oral anticoagulants (NOACs), warfarin, and vitamin K antagonists.