The following are the major diseases or complications that may be contributed to by SARS-CoV-2 (novel coronavirus: 2019-nCoV) or COVID-19 (corona virus disease 2019):
Respiratory System (J00-J99)
- Atypical pneumonia (pneumonia): COVID-19 (Engl. Corona virus disease 2019; synonym: Engl. Novel coronavirus-infected pneumonia (NCIP))Note: Occurrence also possible in children (median 3 years; 1-7 years).
- COVID-19 pneumonia runs a biphasic course in hospitalized patients [Leiltin lines: 1].
- L phase: patients are often severely hypoxemic (“lack of oxygen in the blood (concerning hypoxemia)”) but still have comparatively little subjective dyspnea and compliance (distensibility) of the lungs is still high.
- H phase: there is a severe deterioration of blood gases, lung compliance decreases, cardiovascular (“cardiovascular”) organ complications occur and patients require intensive care.
- COVID-19 pneumonia runs a biphasic course in hospitalized patients [Leiltin lines: 1].
- ARDS (acut respiratory distress syndrome; respiratory distress syndrome) – acute respiratory failure in previously lung-healthy humans (onset at a median of 8 days after initial symptoms).
- Pneumothorax – collapse of the lung caused by an accumulation of air between the visceral pleura (lung pleura) and the parietal pleura (chest pleura) (about 1 percent of hospitalized patients)
Blood-forming organs – immune system (D50-D90).
- Coagulopathy – disorder of blood clotting.
Endocrine, nutritional, and metabolic diseases (E00-E90).
- Diabetes mellitus (in this case, new-onset diabetes) – due to damage to beta cells (pancreatic islet cells that produce the hormone insulin); these are damaged because they produce the protein ACE2, which is also the binding site for SARS-CoV-2 to enter cells
- Diabetic ketoacidosis – severe metabolic derailment (ketoacidosis) in the absence of insulin); mainly in diabetes mellitus type 1.
- Metabolic acidosis (metabolic hyperacidity), decompensated.
- Thyroiditis (inflammation of the thyroid gland), subacute.
Skin and subcutaneous (L00-L99)
- Urticaria (hives)
Infectious and parasitic diseases (A00-B99).
- Bacterial infections (due tosuperinfection/secondary infection with bacteria).
Circulatory system (I00-I99)
- Apoplexy (stroke)
- Cor pulmonale, acute – dilatation (widening) and/or hypertrophy (enlargement) of the right ventricle (main chamber) of the heart due to pulmonary hypertension (increase in pressure in the pulmonary circulation.
- Endotheliitis (inflammation of the endothelial cells/cells lining the inside of blood vessels).
- Heart failure (cardiac insufficiency)
- Cardiac arrhythmias
- Cardiomyopathy (heart muscle disease; in this case: acute heart damage).
- Myocarditis (inflammation of the heart muscle)
- Myocarditis, fulminant – as early complications of SARS-CoV-2 infection.
- Myocardial changes with chest pain, palpitations, and chest tightness after hospital discharge; Magnetic resonance imaging: abnormal changes in myocardium such as myocardial edema, fibrosis, and impaired right ventricular function as (late) manifestations of SARS-CoV-2 infection; Limitation: larger studies are needed to determine with certainty that this is cardiac late complication of SARS-CoV-2 infection.
- Pulmonary embolism (LE) – one in five COVID-19 patients requiring intensive care had a pulmonary embolism at a median of day 6 (days 1-18)
- Sudden cardiac death (PHT).
- RV dysfunction (right ventricular dysfunction) with increased pulmonary vascular resistance (vascular resistance in the pulmonary circulation), characterized by waning pulmonary acceleration time (AT)
- Thrombosis (vascular disease in which a blood clot (thrombus) forms in a vein) – deep vein thrombosis (DVT); risk for COVID-19 patients to develop VTE later in the course of disease:
- Padua prediction score (used to stratify risk for VTE) of ≥ 4.
- CURB-65 score between 3-5 (see “Physical examination” below).
- D-dimer levels ˃ 1.0 µg/ml at hospital admission.
- Thromboembolism (occlusion of a blood vessel by a detached thrombus/blood clot)]
Musculoskeletal system and connective tissue (M00-M99).
- Atypical Kawasaki syndrome (belongs to the vasculitis/vasculitis group; CDC terminology: “Multisystem Inflammatory Syndrome in Children (MIS-C) Associated with Coronavirus Disease 2019”).
- With a much more severe course than is usually seen in Kawasaki syndrome; it affects mainly young children; clinical picture: onset with high fever that persists for at least 5 days, accompanied by exanthema (rash), conjunctivitis (conjunctivitis), cervical lymphadenopathy (enlargement of the lymph nodes in the neck), brittle paint lips, and stomatitis (inflammation of the oral mucosa) with a strawberry tongue.
- Toxic shock syndrome (TSS; severe circulatory and organ failure) occurred in 5 of the 10 children in the cases, 6 children were diagnosed with cardiac dysfunction, and 2 children were observed to have aneurysms (balloon-like bulging of the wall of blood vessels) in the coronary arteries (arteries that supply the heart muscle).
Psyche – Nervous System (F00-F99; G00-G99).
- Encephalitis (inflammation of the brain).
- Anxiety disorders due to quarantine
- Depression due toquarantine
- Guillain-Barré syndrome (GBS; synonyms: Idiopathic polyradiculoneuritis, Landry-Guillain-Barré-Strohl syndrome); two courses: acute inflammatory demyelinating polyneuropathy or chronic inflammatory demyelinating polyneuropathy (peripheral nervous system disease); idiopathic polyneuritis (diseases of multiple nerves) of spinal nerve roots and peripheral nerves with ascending paralysis and pain; usually occurs after infections, eg. e.g., after bacterial intestinal infection or infection with cytomegalovirus (CMV); while this often takes 2-4 weeks for infection-associated GBS to occur, in reported cases of SARS-CoV-2 infection, this severe complication occurred after only 5-10 days.
- Hypoxic encephalopathy (brain dysfunction due to oxygen deprivation).
- Insomnia (sleep disturbance) due to quarantine.
- Meningoencephalitis (combined inflammation of the brain (encephalitis) and meninges (meningitis)).
Pregnancy, childbirth and puerperium (O00-O99).
- Premature birth (3 times more common)
Symptoms and abnormal clinical and laboratory findings not elsewhere classified (R00-R99)
- Diarrhea (diarrhea)
- Dyspnea (shortness of breath), severe (100% of those who died and in one-third of survivors)
- Exanthema (skin rash), erythematous (“accompanied by redness of the skin”).
- Fatigue (tiredness) – feeling of persistent tiredness, exhaustion, and listlessness (for weeks after recovery; severity is independent of the severity of the original illness)
- Taste disturbances (dysgeusia; here: loss of taste) (in the later infection phase).
- Hematuria (blood in the urine)
- Hyperglycemia (hyperglycemia)
- Cardiogenic shock – form of shock caused by pumping failure of the heart.
- Nausea (nausea)
- Petechiae (flea-like bleeding)
- Proteinuria (increased excretion of protein in the urine).
- Sepsis, viral (in this case, generalized inflammation caused by viral invasion of the bloodstream; onset: 9 days after hospital admission)
- Septic shock (70% of those who died, but none of those who survived).
- Olfactory dysfunction (dysosmia; in this case, loss of smell)-occurrence in the later phase of infection; anosmia (absence of sense of smell) often persists beyond the end of symptoms; SARS-CoV-2, after its entry into the nasal mucosa, destroys the supporting cells of the olfactory epithelium in addition to the normal epithelia.
- Vertigo (dizziness)
Genitourinary system (N00-N99)
- Acute renal failure (ANV)
- Nephritis (kidney inflammation) – virus affects tubular epithelial cells (epithelial cells that form the anterior part of the tubule in the kidney, the proximal tubule) and podocytes (cells of the renal corpuscles that form the inner leaflet of Bowman’s capsule and are therefore, together with the basement membrane, of particular importance for the filtering function of the kidneys)
Digestive system (K00-K93)
- Ischemic enteritis (inflammation of the small intestine based on reduced blood flow) – with patchy necrosis (death of cells), some of which was confined to the mucosa (mucous membrane) and some of which extended to the entire intestinal wall. The cause is believed to be thrombosis of the small blood vessels as a result of infection and damage to the endothelia (layer of cells on the inner surface of the blood and lymph vessels).
Further
- Cognitive deficits in severely affected COVID-19 patients.
- Death: median after 19 days
- Catheter-associated embolism – embolism (blockage of a blood vessel) caused by intravascular (“located in a blood vessel”) catheters.
- Superinfection
Prognostic factors
- Genetic risk depending on gene polymorphisms:
- People with genotype E4 in the gene for apolipoprotein E: increased risk of severe course of SARS-CoV-2 infection if they do not (yet) have dementia. Allele E4 interferes with macrophage (phagocyte) function; The gene is expressed in type 2 alveolar cells (cells of the alveoli), which are among the first targets of SARS-CoV-2 in the human body.
- Higher risk of worse outcome for A-positive individuals (OR = 1.45) and protective effect for blood type O (OR = 0.65).
- Age over 60 years (HR: 2.40).
- Male gender (HR: 1.59)
- Men (70% of those who died and 59% of those who survived) and people >70 years of age; in England, more than 90% of all people who died from COVID-19 were older than 60 years of age
- Pre-existing conditions
- Overweight (BMI ≥ 25; obesity) – obesity with a body mass index (BMI) of more than 35 kg/m² (HR: 1.40-1.92)
- Diabetes mellitus (HR: 1.95).
- Stroke or pre-existing dementia (HR: 2.16) Other pre-existing neurological disease (HR: 2.58).
- Diseases that were associated with immunosuppression or related therapy (HR: 1.70)
- Patients with trisomy 21
- High sequential organ failure assessment (SOFA) score 4.5 vs 2.2, respectively.
- Prognosis score CRB-65 and CURB-65
- Laboratory parameters
- D-dimer levels: > 1 μg/L; also a continuous increase.
- Lymphopenia (lymphocyte deficiency): < 1×109 per liter (40% of patients); in survivors, the number increased continuously after about ten days on average to 1.43×109 per liter
- Alanine aminotransferase (ALT; GPT) ↑
- Creatinine kinase (CK) ↑
- IL-6 (interleukin-6) ↑
- Creatinine ↑
- LDH ↑
- Prothrombin time ↑
- Procalcitonin ↑
- Serum ferritin ↑
- Troponin T ↑ (large troponin increase is a poor prognostic sign).
- Other laboratory parameters
- Cortisol ↑ – associated with less favorable course of COVID-19 infection.
- EGFR: renal dysfunction with an estimated glomerular filtration rate (eGFR) of less than 30 (HR: 2.52).
- Fever > 10 days (decrease in fever after approximately ten days is considered the first positive sign).
- Cough and dyspnea (shortness of breath) > 10 days.
- Many comorbidities (concomitant diseases): hypertension (high blood pressure), diabetes mellitus, and coronary artery disease (CAD; coronary artery disease) occurred about twice as frequently among the deceased as among the survivors
- In England, elevated blood pressure was not associated with increased risk of death
- Overweight (BMI ≥ 25; obesity).
- Nutritional status: malnutrition and malnutrition worsen the prognosis in COVID-19.
- Smokers
- Invasive mechanical ventilation
- 32 patients required invasive mechanical ventilation, of whom 31 eventually died
- According to the UK Intensive Care National Audit and Research Center (ICNARC), only 1 in 3 patients could be discharged alive after mechanical ventilation.The 30-day mortality of patients receiving intensive care was 51.6%; a comparison group of patients whose pneumonia (lung infection) was caused by other viruses was 22.0%
COVID-19 risk score (HA2T2 score)
Independent predictors of 30-day mortality in COVID-19.
| Parameter | Score | |
| Troponin elevation | 2 | |
| Age | 65-75 years | 1 |
| ≥ 75 years | 2 | |
| Hypoxia on hospital admission | 1 | |
Interpretation
- <3 points: 30-day mortality rate of 5.9
- ≥ 3 points: 30-day mortality of 43.7%.
Limitation: patient data are from a time when New York was severely affected by the coronavirus pandemic and thus inadequately reflect the current situation.
