However, the use of bleeding time in diagnosis is discouraged by the American Society of Hematology practice guidelines and a normal bleeding time does not exclude a platelet disorder.Bone marrow examination may be performed on patients over the age of 60 and those who do not respond to treatment, or when the diagnosis is in doubt. On examination of the marrow, an increase in the production of megakaryocytes may be observed  and may help in establishing a diagnosis of ITP. An analysis for anti-platelet antibodies is a matter of clinicians preference, as there is disagreement on whether the 80 percent specificity of this test is sufficient to be clinically useful. Treatment
With rare exceptions, there is usually no need to treat based on platelet counts. Many older recommendations suggested a certain platelet count threshold (usually somewhere below 20.0/µl) as an indication for hospitalization or treatment. Current guidelines recommend treatment only in cases of significant bleeding. Treatment recommendations sometimes differ for adult and pediatric ITP. Steroids
Initial treatment usually consists of the administration of corticosteroids, a group of medications that suppress the immune system. The dose and mode of administration is determined by platelet count and whether there is active bleeding: in urgent situations, infusions of dexamethasone or methylprednisolone may be used, while oral prednisone or prednisolone may suffice in less severe cases. Once the platelet count has improved, the dose of steroid is gradually reduced while the possibility of relapse is monitored. 60–90 percent will experience a relapse during dose reduction or cessation.
Schneckenbecken dysplasia is a rare pre-natally fatal hereditary autosomal recessive condition which affects the bones and pre-natal growth. Signs and symptoms
Fetuses with the condition typically have a hypoplastic iliac bone which resembles a snail, short ribs, short neck, shortened and widened (dysplastic) fibula bones, premature ossification of the tarsus, shortened and broadened long bones which resemble a dumbbell, hypoplastia and flattening vertebrae, macrocephaly, dolichocephaly, toenail hypoplasia, flattening of the malar prominence, and micromelic (short-limbed) dwarfism. Complications
Fetuses homozygous for this condition typically die before being born, and because of this they dont usually live to experience the complications of the disease. Genetics
This condition is typically caused by loss-of-function mutations in the SLC35D1 gene, located in chromosome 1. These mutations are inherited in an autosomal recessive manner. Diagnosis
This condition can be diagnosed through the following methods:

Ultrasound (due to its prenatally fatal nature)
Whole genome sequencing
Physical examination
Post-mortem autopsy

Treatment
There is no cure for this disorder, and attempted treatment will always be ineffective due to this conditions lethal nature. Prevalence
According to OrphaNet, less than 20 cases have been reported. History
This condition was first discovered in 1986 by Knowles et al. when they described 5 fetuses born to a consanguineous, first-cousin Asian couple. The couple in question went through 13 pregnancies, these pregnancies consisted of 4 successful pregnancies which resulted in healthy children, 5 pregnancies which resulted in dead dwarf babies, 3 pregnancies which ended in miscarriage, and 1 pregnancy which was clinically aborted after the pre-natal detection of dwarfism.