Congenital oculomotor palsy
The origins of the vast majority of congenital oculomotor palsies are idiopathic. There is some evidence of a familial tendency to the condition, particularly to a partial palsy involving the superior division of the nerve with an autosomal recessive inheritance. The condition can also result from aplasia or hypoplasia of one or more of the muscles supplied by the oculomotor nerve. It can also occur as a consequence of severe birth trauma. Acquired oculomotor palsy
Vascular disorders such as diabetes, heart disease, atherosclerosis and aneurysm, particularly of the posterior communicating artery
Space occupying lesions or tumours, both malignant and non-malignant
Inflammation and infection
Trauma
Demyelinating disease (multiple sclerosis)
Autoimmune disorders such as myasthenia gravis
Post-operatively as a complication of neurosurgery
Cavernous sinus thrombosis

Mechanism
As the pair of oculomotor nerves arises from different subnuclei in the midbrain, courses through different structures in the brain and branches into superior and inferior divisions after exiting the cavernous sinuses, any lesions along its path will produce different pathological features of the third nerve palsy. The parasympathetic aspect of the nerve (which constricts pupils and thicken the lens) is located on the nerve surface, supplied by pial blood vessels. The nerves core contains the main trunk of the oculomotor nerve, supplied by vasa vasorum. Thus pathologies affecting the nerves core without affecting the superficial part of the nerve (thus sparing the pupillary reflex) are known as "medical" oculomotor nerve palsy.
Investigation
In a hospital, physicians respond to a case of hypovolemic shock by conducting these investigations:
Blood tests: U+Es/Chem7, full blood count, glucose, blood type and screen
Central venous catheter
Arterial line
Urine output measurements (via urinary catheter)
Blood pressure
SpO2 oxygen saturation monitoring

Stages
Untreated hypovolemia can lead to shock (see also: hypovolemic shock). Most sources state that there are 4 stages of hypovolemia and subsequent shock; however, a number of other systems exist with as many as 6 stages.The 4 stages are sometimes known as the "Tennis" staging of hypovolemic shock, as the stages of blood loss (under 15% of volume, 15–30% of volume, 30–40% of volume and above 40% of volume) mimic the scores in a game of tennis: 15, 15–30, 30–40 and 40. It is basically the same as used in classifying bleeding by blood loss. The signs and symptoms of the major stages of hypovolemic shock include:

Treatment
Field care
The most important step in treatment of hypovolemic shock is to identify and control the source of bleeding.Medical personnel should immediately supply emergency oxygen to increase efficiency of the patients remaining blood supply. This intervention can be life-saving.Also, the respiratory pump is especially important during hypovolemia as spontaneous breathing may help reduce the effect of this loss of blood pressure on stroke volume by increasing venous return.The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen the way blood does—however, researchers are developing blood substitutes that can.