Surgical complications can develop and include:
Allergic shock due to anesthetics
A paradoxical reaction to a drug
Infection

Cause
The development of TOA is thought to begin with the pathogens spreading from the cervix to the endometrium, through the salpinx, into the peritoneal cavity and forming the tubo-ovarian abscess with (in some cases) pelvic peritonitis. TOA can develop from the lymphatic system with infection of the parametrium from an intrauterine device (IUD). Bacteria recovered from  TOAs are Escherichia coli, Bacteroides fragilis, other Bacteroides species, Peptostreptococcus, Peptococcus, and aerobic streptococci. Long term IUD use is associated with TOA. Actinomyces is also recovered from TOA. Diagnosis
Laparoscopy and other imaging tools can visualize the abscess. Physicians are able to make the diagnosis if the abscess ruptures when the woman begins to have lower abdominal pain that then begins to spread. The symptoms then become the same as the symptoms for peritonitis. Sepsis occurs, if left untreated. : 103  Ultrasonography is a sensitive enough imaging tool that it can accurately differentiate between pregnancy, hemorrhagic ovarian cysts, endometriosis, ovarian torsion, and tubo-ovarian abscess. Its availability, the relative advancement in the training of its use, its low cost, and because it does not expose the woman (or fetus) to ionizing radiation, ultrasonography an ideal imaging procedure for women of reproductive age. Prevention
Risk factors have been identified which indicate what women will be more likely to develop TOA. These are: increased age, IUD insertion, chlamydia infection, and increased levels of certain proteins (CRP and CA-125) and will alert clinicians to follow up on unresolved symptoms of PID.
Mitochondrial disease leading to neurodegeneration is likely, at least on some level, to involve all of these functions.There is strong evidence that mitochondrial dysfunction and oxidative stress play a causal role in neurodegenerative disease pathogenesis, including in four of the more well known diseases Alzheimers, Parkinsons, Huntingtons, and amyotrophic lateral sclerosis.Neurons are particularly vulnerable to oxidative damage due to their strong metabolic activity associated with high transcription levels, high oxygen consumption, and weak antioxidant defense. DNA damage
The brain metabolizes as much as a fifth of consumed oxygen, and reactive oxygen species produced by oxidative metabolism are a major source of DNA damage in the brain. Damage to a cells DNA is particularly harmful because DNA is the blueprint for protein production and unlike other molecules it cannot simply be replaced by re-synthesis. The vulnerability of post-mitotic neurons to DNA damage (such as oxidative lesions or certain types of DNA strand breaks), coupled with a gradual decline in the activities of repair mechanisms, could lead to accumulation of DNA damage with age and contribute to brain aging and neurodegeneration. DNA single-strand breaks are common and are associated with the neurodegenerative disease ataxia-oculomotor apraxia. Increased oxidative DNA damage in the brain is associated with Alzheimers disease and Parkinsons disease. Defective DNA repair has been linked to neurodegenerative disorders such as Alzheimers disease, amyotrophic lateral sclerosis, ataxia telangiectasia, Cockayne syndrome, Parkinsons disease and xeroderma pigmentosum. Axonal transport
Axonal swelling, and axonal spheroids have been observed in many different neurodegenerative diseases.