It is given by intramuscular injection as part of modern routine antenatal care. Despite excellent results, the medication retains an FDA Pregnancy Category C.RhIG is recommended in the UK after antenatal pathological events that are likely to cause a feto–maternal hemorrhage. Applicable pathologic events include accidents which may induce fetomaternal hemorrhage (motor vehicle accidents, falls, abdominal trauma), following obstetric/gynecologic procedures during pregnancy, and at the time of threatened- or spontaneous-/elective abortions, regardless of gestational age. There is insufficient evidence that the use of Rho(D) immune globulin after a spontaneous miscarriage is needed and a Cochrane review recommends that local practices be followed.In an RhD negative mother, RhIG can prevent temporary sensitization of the maternal immune system to RhD antigens, which can cause rhesus disease in the current or in subsequent pregnancies. With the widespread use of RhIG, Rh disease of the fetus and newborn has almost disappeared in the developed world. The risk that an RhD negative mother can be alloimmunized by a RhD positive fetus can be reduced from approximately 16% to less than 0.1% by the appropriate administration of RhIG.Rh immune globulin is composed of IgG antibodies and therefore is able to cross the placenta. In rare cases this can cause a baby to have a weakly positive direct antiglobulin test (DAT) due to sensitization of fetal cells from mothers who have received multiple doses of RhIG. However, no treatment is necessary as the clinical course is benign.
Idiopathic pure sudomotor failure (IPSF) is the most common cause of a rare disorder known as acquired idiopathic generalized anhidrosis (AIGA), a clinical syndrome characterized by generalized decrease or absence of sweating without other autonomic and somatic nervous dysfunctions and without persistent organic cutaneous lesions.The term IPSF was first introduced in 1994 after researchers at Saitama Medical School speculated the primary lesion sites in patients were within cholinergic receptors of the sweat glands. The term IPSF represent a distinct subgroup of AIGA without sudomotor neuropathy or sweat gland failure. Clinical features
Early onset in life
Acute or sudden onset
Concomitant sharp pain or cholinergic urticaria over the entire body
Absence of other autonomic dysfunction
Elevated serum IgE levels
Marked response to glucocorticoids
Preserved apocrine sweating (adrenergic innervation)

Pathology
Intracutaneous injection of pilocarpine (sweat gland stimulant) is known to evoke no sweat response, indicating that lesions are on the post-synaptic side of the nerve-sweat gland junction.The proposed pathomechanisms of idiopathic pure sudomotor failure include:

A deficit within muscarinic cholinergic receptors of the eccrine sweat glands. Interference in acetylcholine transmission to cholinergic receptors. A cross-reactive immune response which interferes with cholinergic transmission in the eccrine glands. Components of an immediate-type allergy (based on the dramatic resumption of axon reflex sweating following glucocorticoid treatment). Diagnosis
Management
Treatment of AIGA almost always consists of steroid pulse therapy or high-dose oral steroids and is not consistently effective. Much remains unclear regarding the reasons for recurrent anhidrosis.