acute kidney injury
Frequent in severe disease. May be caused by dehydration initially, but may be a consequence of disseminated intravascular coagulation or direct damage to the kidneys by the Ebola virus in later stages. Early recognition by monitoring urine output and blood biochemistry enables prompt action to be taken.
Aetiology in Ebola virus infection is still not well understood. Multiple factors may contribute, including: bacterial sepsis, possibly through gut translocation of bacteria; a direct effect of the virus; disseminated intravascular coagulation; and haemorrhage. Management follows the same principles as for bacterial sepsis.
disseminated intravascular coagulation
Predisposes patient to bleeding complications. Major bleeding occurs infrequently, but is a manifestation of advanced infection that is usually fatal. When available, fresh whole blood or platelet and plasma transfusions should be given according to local protocols guided by clinical and laboratory (if available) indicators (e.g., haemoglobin, haematocrit, INR).
Survivors and orphans of those who have died face stigma and ostracism in many communities. This can be associated with psychological issues, including depression, anxiety, post-traumatic stress disorder, obsessive-compulsive disorder, substance addiction, and suicidal tendencies. Approximately 20% of survivors are diagnosed with depression.
late convalescence complications
Patients who survive commonly exhibit a protracted recovery characterised by asthenia, weight loss, and migratory arthralgia. Skin desquamation and transient hair loss also occur frequently.
Late manifestations during convalescence are uncommon but may include orchitis, myelitis, parotitis, pancreatitis, hepatitis, psychosis, and hearing loss/tinnitus. Survivors are also at risk of uveitis (anterior, posterior, or panuveitis), which may lead to secondary structural complications, vision impairment, or blindness. One retrospective, uncontrolled, cross-sectional study found that approximately 28% of survivors developed Ebola-associated uveitis, and 3% developed Ebola-associated optic neuropathy. In patients with uveitis, 38.5% of patients were blind. One survivor had acute uveitis with detection of viable Ebola virus 14 weeks after the onset of infection and 9 weeks after the clearance of the virus from the blood. Unilateral white cataracts and a novel retinal lesion following the anatomical distribution of the optic nerve axons have also been reported.
One expatriate healthcare worker presented with Ebola virus meningoencephalitis (RT-PCR of CSF and plasma were positive for Ebola virus) 9 months after recovering from severe primary Ebola virus disease in 2015. Full genome sequencing was performed comparing the initial virus detected in the blood at presentation to the virus detected in the CSF at 10 months, revealing no changes in the coding regions. The authors of this study concluded that they were not able to discern whether the virus remained latent and reactivated, or continually replicated, but were able to confirm, through sequencing, that an immune escape variant had not emergedA case of late-onset encephalitis and polyarthritis has also been reported.
The aetiology of these manifestations is unclear but could be related to immune complex phenomena or the persistence of Ebola virus in immune-privileged sites.
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