Top videos

• All Time
• Today
• This week
• This month
• This year

Foreceps Delivery Birth Video

The term chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) has been used to identify patients with a chronically progressive or relapsing symmetric sensorimotor disorder with cytoalbuminologic dissociation and interstitial and perivascular endoneurial infiltration by lymphocytes and macrophages. It can be considered the chronic equivalent of acute inflammatory demyelinating polyradiculoneuropathy, the most common form of Guillain-Barré syndrome. Signs and symptoms CIDP typically starts insidiously and evolves slowly, in either a slowly progressive or a relapsing manner, with partial or complete recovery between recurrences; periods of worsening and improvement usually last weeks or months. Most experts consider the necessary duration of symptoms to be greater than 8 weeks for the diagnosis of CIDP to be made. Symptoms reported include the following: Preceding infection (infrequent) Initial limb weakness, both proximal and distal Sensory symptoms (eg, tingling and numbness of hands and feet) Motor symptoms (usually predominant) In about 16% of patients, a relatively acute or subacute onset of symptoms In children, usually a more precipitous onset of symptoms Symptoms of autonomic system dysfunction (eg, orthostatic dizziness) Pertinent physical findings are limited to the nervous system, except when the condition is associated with other diseases. Such findings may include the following. Signs of cranial nerve (CN) involvement (eg, facial muscle paralysis or diplopia) Gait abnormalities Motor deficits (eg, symmetric weakness of both proximal and distal muscles in upper and lower extremities) Diminished or absent deep tendon reflexes Sensory deficits (typically in stocking-glove distribution) Impaired coordination See Clinical Presentation for more detail. Diagnosis Laboratory studies that may be helpful include the following: Cerebrospinal fluid analysis: Elevated protein levels are common (80% of patients); 10% of patients also have mild lymphocytic pleocytosis and increased gamma globulin Complete blood count (CBC), erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA) level, biochemistry profile, and serum and urine immunoelectrophoresis (to exclude associated systemic disorders) In certain instances, genetic testing Other tests and procedures that may be warranted are as follows: MRI of the spine with gadolinium enhancement Electromyography (EMG) is a critical test to determine whether the disorder is truly a peripheral neuropathy and whether the neuropathy is demyelinating Peripheral (sural) nerve biopsy (see the image below): This is considered when the diagnosis is not completely clear, when other causes cannot be excluded, or when profound axonal involvement is observed on EMG; biopsy was once commonly recommended for most patients before immunosuppressive therapy, but current guidelines no longer recommend it

Umbilical Cord Around Fetal Neck During Delivery

Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body. The name myasthenia gravis, which is Latin and Greek in origin, literally means "grave muscle weakness."

Anatomy of The Superficial Dissection of The Upper and Lower Limbs

Rectal Examination

Asthma Mechanism 3D

Congestive Heart Failure Animation

Carotid Endarterectomy Surgery

This shows how to observe the movement pattern of a baby for motor abnormalities

Psychomotor learning is demonstrated by physical skills such as movement, coordination, manipulation, dexterity, grace, strength, speed; actions which demonstrate the fine motor skills such as use of precision instruments or tools. Psychomotor ability refers to a wide range of actions involving physical movement related to conscious cognitive processing. Psychomotor ability may be measured by accuracy or speed (reaction time)

The World Health Organization's official handwashing demonstration: the full soap-and-water technique, surface by surface. The Key Steps checklist on this page follows the WHO sequence in order. General hygiene education — follow your institution's hand-hygiene policy.

How to insert Endotracheal tube in children

Pediatric Lumbar puncture

Proximal Hypospadia repaired by Tube Onaly Urethroplasty

DRE

A video showing breast examination after breast implants

Vacuum Extraction Childbirth Video with ventouse

Hernia Repair with Prolene Hernia System

Most intact aortic aneurysms do not produce symptoms. As they enlarge, symptoms such as abdominal pain and back pain may develop. Compression of nerve roots may cause leg pain or numbness. Untreated, aneurysms tend to become progressively larger, although the rate of enlargement is unpredictable for any individual. Rarely, clotted blood which lines most aortic aneurysms can break off and result in an embolus. They may be found on physical examination. Medical imaging is necessary to confirm the diagnosis. Symptoms may include: anxiety or feeling of stress; nausea and vomiting; clammy skin; rapid heart rate. In patients presenting with aneurysm of the arch of the aorta, a common symptom is a hoarse voice as the left recurrent laryngeal nerve (a branch of the vagus nerve) is stretched. This is due to the recurrent laryngeal nerve winding around the arch of the aorta. If an aneurysm occurs in this location, the arch of the aorta will swell, hence stretching the left recurrent laryngeal nerve. The patient therefore has a hoarse voice as the recurrent laryngeal nerve allows function and sensation in the voicebox. Abdominal aortic aneurysms, hereafter referred to as AAAs, are the most common type of aortic aneurysm. One reason for this is that elastin, the principal load-bearing protein present in the wall of the aorta, is reduced in the abdominal aorta as compared to the thoracic aorta (nearer the heart). Another is that the abdominal aorta does not possess vasa vasorum, hindering repair. Most are true aneurysms that involve all three layers (tunica intima, tunica media and tunica adventitia), and are generally asymptomatic before rupture. The most common sign for the aortic aneuysm is the Erythema nodosum also known as leg lesions typically found near the ankle area. The prevalence of AAAs increases with age, with an average age of 65–70 at the time of diagnosis. AAAs have been attributed to atherosclerosis, though other factors are involved in their formation. An AAA may remain asymptomatic indefinitely. There is a large risk of rupture once the size has reached 5 cm, though some AAAs may swell to over 15 cm in diameter before rupturing. Before rupture, an AAA may present as a large, pulsatile mass above the umbilicus. A bruit may be heard from the turbulent flow in a severe atherosclerotic aneurysm or if thrombosis occurs. Unfortunately, however, rupture is usually the first hint of AAA. Once an aneurysm has ruptured, it presents with a classic pain-hypotension-mass triad. The pain is classically reported in the abdomen, back or flank. It is usually acute, severe and constant, and may radiate through the abdomen to the back. The diagnosis of an abdominal aortic aneurysm can be confirmed at the bedside by the use of ultrasound. Rupture could be indicated by the presence of free fluid in potential abdominal spaces, such as Morison's pouch, the splenorenal space (between the spleen and left kidney), subdiaphragmatic spaces (underneath the diaphragm) and peri-vesical spaces. A contrast-enhanced abdominal CT scan is needed for confirmation. Only 10–25% of patients survive rupture due to large pre- and post-operative mortality. Annual mortality from ruptured abdominal aneurysms in the United States alone is about 15,000. Another important complication of AAA is formation of a thrombus in the aneurysm.