The diaphragm is supplied by the phrenic nerve which has a long intra-thoracic course. Involvement of this nerve anywhere in its course is a common cause of paralysis of the diaphragm. The paralysed dome is pushed up by the intra-abdominal pressure. It moves paradoxically with respiration i.e, during inspiration, it is drawn up and vice versa. Diaphragmatic paralysis may be unilateral or bilateral.
Causes of unilateral paralysis
Birth injuries, viral infections such as Herpes Zoster, Carcinomatous infiltration by bronchogenic carcinoma, diphtheric paralysis, and injury to the nerve due to trauma or surgical avulsion are the common causes. The condition may be asymptomatic, detected during physical examination or by radiology. Sometimes left-sided paralysis may produce gaseous dyspepsia.
Causes of bilateral paralysis
This may result from poliomyelitis, cervical cord lesions, motor neuron disease, muscular dystrophies, myasthemia gravis and Gulliam-Barre’ syndrome. Rarely rheumatic fever, typhoid, penumonia, mediastinitis, pericarditis, and encephalitis lethargical may lead to diaphragmatic paralysis.
In bilateral diaphragmatic paralysis dyspnea may occur because of ventilatory insufficiency. During inspiration, the lower part of the Chest moves horizontally, the subcostal angle widens, and the epigastrium and hypochondria recede. Absence of the normal peeling movements of the diaphragm visible on the thoracic cage is known as “Littens sign”. Abdomen is drawn in during inspiration.
Radiologically, the dome of the diaphragm is seen to be elevated. Other conditions such as pulmonary fibrosis, atelectasis and eventration of the diaphragm also cause elevation of the dome. In diaphragmatic paralysis, the movement is paradoxical. whereas in pulmonary fibrosis and atelectasis, the movement of the elevated diaphragm is considerable restricted.
Eventration of the diaphragm
It is a condition in which the diaphragm is unusually elevated and atrophic. This may be a congenital or acquired condition. In eventration also, the movement is paradoxical. The absence of any underlying cause and persistence over several years should suggest the possibility of eventration.
Treatment: Respiratory embarrassment caused by acute diaphragmatic paralysis may have to be treated by intensive respiratory care and ventilatory support.
The diaphragm acts as a musculotendinous partition between the thoracic and abdominal cavities. The peritoneum and pleura on either side strengthen it further. Infeior vena cave, esophagus, and aorta pass through the diaphragm. The apertures through which they pass are covered and sealed by the serous membranes. When the aperture becomes lax or other defects develop, abdominal contents herniate into the thoracic cavity.
Herniation may be spontaneous without any known cause or it may be traumatic. traumatic hernia is more common on the left side. Though any part may be ruptured, the common site is between the central tendon and ninth rib laterally. Non-traumatic hernias may occur congenitally or may be acquired. Mal-development of the diaphragm or laxity of the apertures occurs in congenital hernias. Four common sites though which herniation occurs are:
1. Esophagu hiatus
2. foramen of Morgagni (between the sternal and costal slips of Origin of the diaphragm)
3. foramen of Bochdalek the (Pleuro-peritoneal hiatus), and
4. through areas of partial absence of the diaphragm.
Among these, in more than 75% cases herniation occurs through the esphagus histus. Herniation of abdominal viscera into the thorax can be clearly delineated by a barium meal follow through examination which will show the presence of stomach and/or intestines above the diaphragm.
This is a common reflex phenomenon resulting from sudden spasmodic invluntary contraction of the diaphragm with the glottis remaining closed. The reflex arc is made up of the vagus and t sensory fibres of the phrenic nerve as the afferent limb and the efferent lim made-up by the motor part of the phrenic nerve. The reflex center is situated in the upper cervical cord. In most cases, the onset and termination of hiccup may be spontaneous and abrupt. Hasty ingestion of food and fluids may trigger off an attack. At times persistent hiccough may be the manifestation of irritation of the phrenic nerve occurring in pericarditis, mediastinitis, and compression by tumors, or during surgery of the thorax and upper abdomen. In most cases, the cause is obscured. Cerebrovascular accidents, encephalitis, brain tumors, renal failure, hepatic failure, diabetic ketoacidosis, respiratory failure and electrolyte disturbances may be accompanied by hiccup. Local irritation of the diaphragm due to gaseous distension of the stomach or intestines, subphrenic abscess, peritonitis and acute myocardial infarction may cause hiccup. Persistent hiccup may be psychogenic. In a gravely ill patient, the muscular effort and discomfort caused by hiccup may hasten death. In hiccup, due to central causes both sides of the diaphragm contract. In conditions caused by local irritation, only one side may contract.
Management: Though many cases stop spontaneously, in resistant cases treatment is unsatisfactory. Simple physical measures such as drinking cold water, pressure over the eye-ball, Valsalva maneuver, pull on the tongue, stimulation of the phrenic nerve by pressure in the neck or rebreathing into a paper bag may stop the hiccup in many cases. Inhalation of 5 to 10% Carbondioxide is effective. Unilateral hiccup can be arrested by local infiltration of the phrenic nerve with procaine. In cases with abdominal distension, aspiration of gastric contents through a nasogastric tube may provide prompt relief. Drug therapy consists of the administration of chlorpromazine 25-50 mg orally or intramuscularly.
Sometimes, the diaphragm manifests paroxysmal wave-like rhythmic movements at rates going up to 100/min or more. The exact mechanism or cause is not clear. When the condition persists, ventilation may be jeopardized. The term ‘diaphragmatic tic’ is given to flutter occurring at a slower rate. Diaphragmatic flutter is seen more frequently in patients recovering from cerebrovascular accidents or encephalitis.
Treatment: The condition responds to anti-convulsant drugs such as dilantin sodium or carbamazepine. In intractable cases temporary phrenic paralysis may have to be induced by crushing the nerve.