A shoulder presentation is a malpresentation at childbirth where the baby is in a transverse lie (its vertebral column is perpendicular to that of the mother), thus the leading part (the part that first enters the birth canal) is an arm, a shoulder, or the trunk. While a baby can be delivered vaginally when either the head or the feet/buttocks are the leading part, it usually cannot be expected to be delivered successfully with a shoulder presentation unless a cesarean section (C/S) is performed. Frequency and causes
Shoulder presentations are uncommon (about 0.5% of births) since, usually, toward the end of gestation, either the head or the buttocks start to enter the upper part of the pelvis, anchoring the fetus in a longitudinal lie. It is not known in all cases of shoulder presentation why the longitudinal lie is not reached, but possible causes include bony abnormalities of the pelvis, uterine abnormalities such as malformations or tumors (fibroids), or other tumors in the pelvis or abdomen. Other factors are a lax abdominal musculature, uterine overdistension (i.e., polyhydramnios), multiple gestation, placenta previa, a small fetus, or a fetus with some abnormality. Further, if the amniotic fluid sac ruptures, the shoulder or arm may become wedged as a shoulder presentation. Diagnosis
Inspection of the abdomen may already give a clue as it is wide from side to side. Usually performing the Leopolds maneuvers will demonstrate the transverse lie of the fetus. Ultrasound examination delivers the diagnosis and may indicate possible causes such as multiple gestation or a tumor.
Alpha-thalassemia (α-thalassemia, α-thalassaemia) is a form of thalassemia involving the genes HBA1 and HBA2. Thalassemias are a group of inherited blood conditions which result in the impaired production of hemoglobin, the molecule that carries oxygen in the blood. Normal hemoglobin consists of two alpha chains and two beta chains; in alpha-thalassemia, there is a quantitative decrease in the amount of alpha chains, resulting in fewer normal hemoglobin molecules. Furthermore, alpha-thalassemia leads to the production of unstable beta globin molecules which cause increased red blood cell destruction. The degree of impairment is based on which clinical phenotype is present (how many genes are affected). Signs and symptoms
The presentation of individuals with alpha-thalassemia consists of:

Cause
Alpha-thalassemias are most commonly inherited in a Mendelian recessive manner. They are also associated with deletions of chromosome 16p. Alpha thalassemia can also be acquired under rare circumstances. Pathophysiology
The mechanism sees that α thalassemias results in decreased alpha-globin production, therefore fewer alpha-globin chains are produced, resulting in an excess of β chains in adults and excess γ chains in newborns. The excess β chains form unstable tetramers called hemoglobin H or HbH of four beta chains. The excess γ chains form tetramers which are poor carriers of O2 since their affinity for O2 is too high, so it is not dissociated in the periphery. Homozygote α0 thalassaemias, where numerous γ4 but no α-globins occur at all (referred to as Hb Barts), often result in death soon after birth. Diagnosis
Diagnosis of alpha-thalassemia is primarily by laboratory evaluation and molecular diagnosis.