Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the novel global coronavirus disease 2019 (COVID-19) disease outbreak. Its pathogenesis is mostly located in the respiratory tract. However, other organs are also affected. Hence, realising how such a complex disturbance affects patients after recovery is crucial. Regarding the significance of control of COVID-19-related complications after recovery, the current study was designed to review the cellular and molecular mechanisms linking COVID-19 to significant long-term signs including renal and cardiac complications, cutaneous and neurological manifestations, as well as blood coagulation disorders. This virus can directly influence on the cells through Angiotensin converting enzyme 2 (ACE-2) to induce cytokine storm. Acute release of Interleukin-1 (IL1), IL6 and plasminogen activator inhibitor 1 (PAI-1) have been related to elevating risk of heart failure. Also, inflammatory cytokines like IL-8 and Tumour necrosis factor-α cause the secretion of von Willebrand factor (VWF) from human endothelial cells and then VWF binds to Neutrophil extracellular traps to induce thrombosis. On the other hand, the virus can damage the blood–brain barrier by increasing its permeability and subsequently enters into the central nervous system and the systemic circulation. Furthermore, SARS-induced ACE2-deficiency decreases [des-Arg9]-bradykinin (desArg9-BK) degradation in kidneys to induce inflammation, thrombotic problems, fibrosis and necrosis. Notably, the angiotensin II-angiotensin II type 1 receptor binding causes an increase in aldosterone and mineralocorticoid receptors on the surface of dendritic cells cells, leading to recalling macrophage and monocyte into inflammatory sites of skin. In conclusions, all the pathways play a key role in the pathogenesis of these disturbances. Nevertheless, more investigations are necessary to determine more pathogenetic mechanisms of the virus.

Summary

Background and objective: The reasons for coagulopathy may be multiple and the identification of the underlying cause is often difficult. Recently, we identified two patients showing characteristics of heparin overdose during surgery. We hypothesised that filling a Shaldon dialysis catheter with heparin prior to closure, so-called heparin lock, might have triggered this coagulation disorder. Therefore, the aim of this in vitro study was to show whether this procedure can lead to an iatrogenic administration of heparin. Methods: A Shaldon catheter (GamCath®; Joka Kathetertechnik, Hechingen, Germany) was hung up in a container filled with NaCl solution 0.9% 5 mL and a heparin lock was simulated. Instead of using heparin solution we injected 1 mL of a KCl solution (1 mol L−1) into the Shaldon catheter, because the measurement of the potassium concentration is faster and more reliable than that of heparin. Ten measurements were taken after fast (0.5 s) and slow (3 s) injection speeds. Results: Although the catheter volume is specified as 1.07 mL, an amount up to 0.51 mL KCl solution on average was detectable in the solution after locking the catheter with 1 mL KCl solution. Conclusions: Following a heparin lock a considerable amount of the injected solution is accidentally administered to the patient. Only 49.1% of the injected volume may remain in the Shaldon catheter. This could lead to an increased risk of coagulopathy.

A 41-year-old multigravida presented at 32 weeks of gestation with polyhydramnios and an anencephalic fetus. Abnormal bleeding as a result of disseminated intravascular coagulation complicated an emergency Caesarean section for severe abdominal pain thought to be due to uterine rupture. Massive transfusion with blood products was necessary and the abdomen packed to control bleeding. The patient was transferred to the intensive care unit where she made a slow but complete recovery. Amniotic fluid embolism with atypical presentation of isolated coagulopathy is the likely diagnosis in this case. The case serves to demonstrate that amniotic fluid embolism may present with symptoms and signs other than the classical pattern of dyspnoea, cyanosis and hypotension.