Respiratory arrest is a sickness caused by apnea (cessation of breathing) or respiratory dysfunction severe enough it will not sustain the body (such as agonal breathing). Prolonged apnea refers to a patient who has stopped breathing for a long period of time. If the heart muscle contraction is intact, the condition is known as respiratory arrest. An abrupt stop of pulmonary gas exchange lasting for more than five minutes may damage vital organs especially the brain, possibly permanently. Lack of oxygen to the brain causes loss of consciousness. Brain injury is likely if respiratory arrest goes untreated for more than three minutes, and death is almost certain if more than five minutes. Damage may be reversible if treated early enough. Respiratory arrest is a life-threatening medical emergency that requires immediate medical attention and management. To save a patient in respiratory arrest, the goal is to restore adequate ventilation and prevent further damage. Management interventions include supplying oxygen, opening the airway, and means of artificial ventilation. In some instances, an impending respiratory arrest could be predetermined by signs the patient is showing, such as the increased work of breathing. Respiratory arrest will ensue once the patient depletes their oxygen reserves and loses the effort to breathe. Respiratory arrest should be distinguished from respiratory failure. The former refers to the complete cessation of breathing, while respiratory failure is the inability to provide adequate ventilation for the bodys requirements.
Children with the more severe form of MPS IV may not live beyond their twenties or thirties. Cause
Morquio syndrome is inherited from an autosomal recessive inherited gene. Every person has two copies of the genes needed to break down keratan sulfate, but only one healthy copy is needed. Both parents pass down one defective copy to their child, resulting in a child with no functional copies of the gene. As such, the body is incapable breaking down keratan sulfate for disposal. The incompletely broken down GAGs remain stored in cells in the body, causing progressive damage. Babies may show little sign of the disease, but as more and more cells become damaged, symptoms start to appear. Diagnosis
Classification
This syndrome has two forms, A and B, referred to as Morquio A and Morquio B syndrome or MPS IVA and MPS IVB. The two forms are distinguished by the gene product involved; Type A involves a malfunction in the GALNS gene, while Type B involves a malfunction of the GLB1 gene. Treatment
The treatment for Morquio syndrome consists of prenatal identification and of enzyme replacement therapy. On 12 February 2014, the US Food and Drug Administration approved the drug elosulfase alfa (Vimizim) for treating Type A. Currently, there is no treatment for Type B.

Prognosis
The lifespan of patients with Morquio syndrome is variable and depends on the subtype. Type A is generally severe, with a life expectancy in the 20s to 30s.