A histologic examination of the tissue would show a lack of ganglionic nerve cells. Diagnostic techniques involve anorectal manometry, barium enema, and rectal biopsy. The suction rectal biopsy is considered the current international gold standard in the diagnosis of Hirschsprungs disease.Radiologic findings may also assist with diagnosis. Cineanography (fluoroscopy of contrast medium passing anorectal region) assists in determining the level of the affected intestines. Treatment
Treatment of Hirschsprungs disease consists of surgical removal (resection) of the abnormal section of the colon, followed by reanastomosis. Colostomy
The first stage of treatment used to be a reversible colostomy. In this approach, the healthy end of the large intestine is cut and attached to an opening created on the front of the abdomen. The contents of the bowel are discharged through the hole in the abdomen and into a bag. Later, when the patients weight, age, and condition are right, the "new" functional end of the bowel is connected with the anus. The first surgical treatment involving surgical resection followed by reanastomosis without a colostomy occurred as early as 1933 by Doctor Baird in Birmingham on a one-year-old boy. Other procedures
The Swedish-American surgeon Orvar Swenson (1909–2012), who discovered the cause of Hirschsprungs, first performed its surgical treatment, the pull-through surgery, in 1948. The pull-through procedure repairs the colon by connecting the functioning portion of the bowel to the anus. The pull-through procedure is the typical method for treating Hirschsprungs in younger patients. Swenson devised the original procedure, and the pull-through surgery has been modified many times.
Platelet storage pool deficiency is a type of coagulopathy characterized by defects in the granules in platelets, particularly a lack of granular non-metabolic adenosine diphosphate. Individuals with adenosine diphosphate deficient storage pool disease present a prolonged bleeding time due to impaired aggregation response to fibrillar collagen. Symptoms and signs
The presentation (signs/symptoms) of an individual with  platelet storage pool deficiency is as follows:
Unusual bleeding(after surgical procedure)
Anemia
Decrease mean platelet volume
Myelodysplasia

Cause
The condition of platelet storage pool deficiency can be acquired  or inherited (genetically passed on from the individuals parents). Some of the causes of platelet storage pool deficiency when acquired are:
Hairy-cell leukemia
Cardiovascular bypass

Mechanism
In terms of the pathophysiology of platelet storage pool deficiency one must consider several factors including the human bodys normal function prior to such a deficiency, such as platelet alpha-granules one of three types of platelet secretory granulePlatelet α–granules are important in platelet activity, α–granules connect with plasma membrane. This in turn increases the size of the platelet. Platelet α–granules have an important role in hemostasis as well as thrombosis. SNARE accessory proteins control the secretion of α–granule. Diagnosis
The diagnosis of this condition can be done via the following:
Flow cytometry
Bleeding time analysis
Platelet aggregation function study:

Types
This condition may involve the alpha granules or the dense granules. Therefore, the following examples include:

Platelet alpha-granules
Gray platelet syndrome
Quebec platelet disorder
Dense granules
δ-Storage pool deficiency
Hermansky–Pudlak syndrome
Chédiak–Higashi syndrome

Treatment
Platelet storage pool deficiency has no treatment however management consists of antifibrinolytic medications if the individual has unusual bleeding event, additionally caution should be taken with usage of NSAIDS

See also
Hypocoagulability
Hypercoagulability

References
Further reading
Sandrock, Kirstin; Zieger, Barbara (2010).