Causes
There are three main causes of PVS (persistent vegetative state):

Acute traumatic brain injury
Non-traumatic: neurodegenerative disorder or metabolic disorder of the brain
Severe congenital abnormality of the central nervous systemPotential causes of PVS are:
Bacterial, viral, or fungal infection, including meningitis
Increased intracranial pressure, such as a tumor or abscess
Vascular pressure which causes intracranial hemorrhaging or stroke
Hypoxic ischemic injury (hypotension, cardiac arrest, arrhythmia, near-drowning)
Toxins such as uremia, ethanol, atropine, opiates, lead, dimethylmercury, endrin, parathion, and colloidal silver
Physical trauma: Concussion, contusion, etc. Seizure, both nonconvulsive status epilepticus and postconvulsive state (postictal state)
Electrolyte imbalance, which involves hyponatremia, hypernatremia, hypomagnesemia, hypoglycemia, hyperglycemia, hypercalcemia, and hypocalcemia
Postinfectious: Acute disseminated encephalomyelitis (ADEM)
Endocrine disorders such as adrenal insufficiency and thyroid disorders
Degenerative and metabolic diseases including urea cycle disorders, Reye syndrome, and mitochondrial disease
Systemic infection and sepsis
Hepatic encephalopathyIn addition, these authors claim that doctors sometimes use the mnemonic device AEIOU-TIPS to recall portions of the differential diagnosis: Alcohol ingestion and acidosis, Epilepsy and encephalopathy, Infection, Opiates, Uremia, Trauma, Insulin overdose or inflammatory disorders, Poisoning and psychogenic causes, and Shock. Diagnosis
Despite converging agreement about the definition of persistent vegetative state, recent reports have raised concerns about the accuracy of diagnosis in some patients, and the extent to which, in a selection of cases, residual cognitive functions may remain undetected and patients are diagnosed as being in a persistent vegetative state. Objective assessment of residual cognitive function can be extremely difficult as motor responses may be minimal, inconsistent, and difficult to document in many patients, or may be undetectable in others because no cognitive output is possible.
Congenital dyserythropoietic anemia (CDA) is a rare blood disorder, similar to the thalassemias. CDA is one of many types of anemia, characterized by ineffective erythropoiesis, and resulting from a decrease in the number of red blood cells (RBCs) in the body and a less than normal quantity of hemoglobin in the blood. CDA may be transmitted by both parents autosomal recessively or dominantly. Signs and symptoms
The symptoms and signs of congenital dyserythropoietic anemia are consistent with:
Tiredness (fatigue)
Weakness
Pale skin

Types
Congenital dyserythropoietic anemia has four different subtypes, CDA Type I, CDA Type II, CDA Type III, and CDA Type IV. CDA type II (CDA II) is the most frequent type of congenital dyserythropoietic anemias. Diagnosis
The diagnosis of congenital dyserythropoietic anemia can be done via sequence analysis of the entire coding region, types I, II, III and IV ( is a relatively new form of CDA that had been found, just 4 cases have been reported) according to the genetic testing registry. Treatment
Treatment of individuals with CDA usually consist of frequent blood transfusions, but this can vary depending on the type that the individual has. Patients report going every 2–3 weeks for blood transfusions. In addition, they must undertake chelation therapy to survive; either deferoxamine, deferasirox, or deferiprone to eliminate the excess iron that accumulates. Removal of the spleen and gallbladder are common. Hemoglobin levels can run anywhere between 8.0 g/dl and 11.0 g/dl in untransfused patients, the amount of blood received by the patient is not as important as their baseline pre-transfusion hemoglobin level.