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Deltasone

By H. Pranck. Southern California University of Professional Studies. 2019.

The white blood cell count is often elevated in the 10 cheap deltasone 5mg with visa,000– 20 order 10 mg deltasone overnight delivery,000 range purchase deltasone 40 mg with mastercard, although this can also indicate the presence of infection purchase 40mg deltasone overnight delivery. Antibiotics are given with infection or even to patients with fever and leukocytosis even if a definite site of infection has not been documented. Ceftriaxone is the preferred agent because it covers Pneumococcus and Haemophilus influenza. Chronic management includes folic acid replacement and vaccinations against Pneumococcus and influenza. That is because the destruction of the cells most often occurs through macrophages in the spleen or by Kupffer cells in the liver. Known causes of autoimmune destruction are from antibodies produced in relationship to various forms of leukemia, especially chronic lymphocytic leukemia, viral infections, lymphoma, collagen vascular diseases like lupus, or in relationship to drugs. The most common drugs are the penicillins, cephalosporins, sulfa drugs, quinidine, alpha- methyldopa, procainamide, rifampin, and thiazides. Cold agglutinin disease is an IgM antibody produced against the red cell in association with malignancies such as lymphoma or Waldenstrom macroglobulinemia and infections such as Mycoplasma or mononucleosis. The onset may be very sudden resulting in fever, syncope, congestive failure, and hemoglobinuria. Mild splenomegaly is present when the disease has been occurring long enough for the time it takes for the spleen to enlarge. Weakness, pallor, jaundice, and dark urine may occur as it can in all forms of hemolysis of sufficient severity. The Coombs test is the specific test that diagnoses autoimmune, cold agglutinin, and often even drug-induced hemolysis. Acanthocytes, a Feature of Several Hematologic and Systemic Diseases Copyright 2007 Gold Standard Multimedia Inc. Most cases of cold agglutinin disease are mild, but in those who have severe disease despite conservative measures, azathioprine, cyclosporine, or cyclophosphamide can be used. Steroids and splenectomy don’t work well with cold agglutinin disease because the destruction occurs in the liver. It is an autosomal dominant disorder where the loss of spectrin in the red cell membrane causes the red cell to form as a sphere, rather than as a more flexible and durable biconcave disc. Hemolysis occurs because the spheres are not able to pass the narrow passages in the spleen. Because the hemolysis occurs in the spleen, there is often splenomegaly and jaundice. Severe anemia occasionally occurs from folate deficiency or Parvovirus B19 infection such as in sickle cell disease. Although spherocytes may be present with autoimmune hemolysis, hereditary spherocytosis has a negative Coombs test. The cells have increased sensitivity to lysis in hypotonic solutions known as an osmotic fragility test. In those with more severe anemia, removal of the spleen will eliminate the site of the hemolysis. Features of Hereditary Spherocytosis Seen on Peripheral Blood Smear Copyright 2007 Gold Standard Multimedia Inc. It is a clonal stem-cell disorder, and so can develop into aplastic anemia and leukemia. Everyone becomes a little acidotic at night because of a relative hypoventilation. In addition to symptoms of anemia, these patients characteristically present with dark urine from intravascular hemolysis. Thrombosis of major venous structures, particularly the hepatic vein (Budd- Chiari syndrome), is a common cause of death in these patients. The hemoglobinuria is most commonly in the first morning urine because the hemolysis occurs more often when patients develop a mild acidosis at night. Hemosiderinuria occurs when the capacity of renal tubular cells to absorb and metabolize the hemoglobin is overwhelmed, and the sloughed off iron-laden cells are found in the urine. Some patients with few or no symptoms require only folic acid and possible iron supplementation. In the anemic patient with signs of hemolysis, prednisone is often given to slow the rate of red blood cell destruction. In the patient with acute thrombosis, thrombolytic therapy (streptokinase, urokinase, or tissue plasminogen activator) is often administered, followed by long-term anticoagulation drugs to help prevent further blood clots. Antiplatelet agents such as aspirin and ibuprofen may also help prevent blood clots. Unfortunately, some patients will continue to develop blot clots despite aggressive anti-coagulation agents. Avoid medications that increase the risk for thrombosis, such as oral birth control pills. Occasionally patients will respond to antithymocyte globulin, but frequently they will continue to require red cell and/or platelet transfusions. The most commonly implicated drugs are sulfa drugs, primaquine, dapsone, quinidine, and nitrofurantoin. A sudden, severe, intravascular hemolysis can occur including jaundice, dark urine, weakness, and tachycardia. There is no specific therapy beyond hydration and transfusion if the hemolysis is severe. Clinical Recall Which of the following clinical scenarios is an indication for an exchange transfusion in a patient with sickle cell anemia? Many things can cause bone marrow failure, but the most common cause of true aplastic anemia is not often determined. Infiltration of the marrow with infections such as tuberculosis or cancer such as lymphoma can cause pancytopenia, but that is not truly aplastic anemia. Patients typically present with bleeding from the thrombocytopenia, and possibly with a combination of the findings associated with deficiencies in all 3 cell lines. The clinical presentation may give a clue to the presence of pancytopenia but is not sufficient to determine a true aplastic anemia by clinical manifestations alone. The absence of a classical association such as benzene, radiation, or chloramphenicol would most certainly not exclude a diagnosis of aplastic anemia. A bone marrow biopsy confirms the diagnosis when alternative etiologies for a pancytopenia are not present. In other words, the marrow is empty of almost all precursor cells as well as evidence of primary or metastatic cancer, infection, or fibrosis. Treatment includes bone marrow transplant when the patient is young and healthy enough to withstand the procedure and there is a donor available (cure rate is 80–90% of patients age <50). When bone marrow transplant is not possible, try immunosuppressive agents: a combination of antithymocyte globulin, cyclosporine, and prednisone (can lead to remission in 60–70% of patients). It is believed that T lymphocytes are primarily causal in the bone marrow failure, so drugs are used to decrease the T- cell response. Most cases of acute leukemia arise with no apparent cause, but there are several well known associations: radiation exposure, benzene, chemotherapeutic agents such as melphalan and etoposide, and some retroviruses. Genetic disorders such as Down syndrome and Klinefelter can cause an increased incidence of leukemia. Enlargement of the liver, spleen, and lymph nodes and bone pain are common at presentation. Rarely, a syndrome of “leukostasis” can occur when the white cell count is extremely elevated. This results from sludging of the leukemic cell in the vasculature, resulting in headache, dyspnea, confusion, and brain hemorrhage. In about 10% of acute leukemias, depression of all 3 cell lines is evident (aleukemic leukemia). None of these will have leukemic blasts circulating in the peripheral blood, however. A bone marrow biopsy showing >20% blasts confirms the diagnosis of acute leukemia. The presence of blasts tells you the patient has acute leukemia, but blast analysis cannot be relied upon to always tell which type is present.

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It should be noted that it is not always due to inadequate intake buy discount deltasone 40 mg on-line, but may be due to excessive loss e generic deltasone 20 mg fast delivery. Cortisone and its derivatives decrease the rate of protein synthesis purchase 10 mg deltasone amex, stabilize liposomal membranes and inhibit the normal inflammatory reaction generic deltasone 10mg visa. High doses of corticoids limit capillary budding, inhibit fibroblast proliferation and decrease the rate of epithelialization. Any agent that inhibit the division of local fibroblasts or epithelial cells should prevent or delay healing. Similarly high doses of radiation especially during first 3 days delay strength of the wound significantly. That is why wounds in the pretibial region take much more time to heal than those in the face, which are well vascularized. Due to infection, fibroblasts face tough time to persist as they have to compete with inflammatory cells and bacteria for oxygen and nutrients. The delicate capillary loops of the granulation tissue and the delicate epithelium are damaged due to movement. Frequent change of dressing also has the same adverse effect and should be avoided. Adhesions to bony surfaces cause delay in wound healing probably by preventing proper wound contraction. Faulty technique of wound closure is obviously responsible for delay in wound healing in many cases. It is a peripheral circulatory failure which results from a discrepancy in the size of the vascular bed and the volume of the intravascular fluid. It is a clinical condition which is characterized by signs and symptoms arising when the cardiac output is insufficient to fill the arterial tree with blood under sufficient pressure to provide all the organs and tissues with adequate blood flow. The characteristic features are decreased filling pressure of the heart, decreased systemic arterial pressure, tachycardia and increased vascular resistance. This is clinically manifested by low cardiac output, tachycardia, low blood pressure and vasoconstriction revealed by cold clammy extremities. In this type of shock there is hypovolaemia due to bleeding both externally and internally (intraperitoneal haemorrhage) from ruptured liver or spleen or from torn vessels of the mesentery alongwith toxic factors resulting from fragments of tissue entering the blood stream. Injury to the chest may cause damage to the respiratory system resulting in hypoxia and shock. Chest injury may also lead to contusion of the heart which may cause failure of pump resulting in shock. This becomes worse with more than 20% of the whole body surface bum in which there occurs generalized capillary leakage in the first day leading to gross hypovolaemia. This causes an intravascular inflammatory response with increase in vascular permeability, which requires large volumes of colloidal and crystaloid fluids for resuscitation. So there is low blood pressure with a normal cardiac output and normal pulse rate and a warm dry skin. In case of spinal anaesthesia and trauma to the spinal cord, low blood pressure can be easily corrected by putting the patient in Trendelenburg position (i. Vasovagal or vasogenic shock is also a part of neurogenic shock in which there is pooling of blood due to dilatation of peripheral vascular system particularly in the limb muscle and in the splanchnic bed. This causes reduced venous return to the heart leading to low cardiac output and bradycardia. This condition can also be corrected by Trendelenburg position which increases cerebral flow and consciousness may be restored. Psychogenic shock, which may follow sudden fright from unexpected bad news or at the sight of horrible accident, is also included in this group. Its effect may vary in intensity from temporary unconsciousness to even sudden death. The left ventricle mainly fails, so that there is over-distension of the right ventricle and ultimately there is increase of back pressure in the pulmonary capillaries. Gradually the vascular volume will increase as a result of salt and water retention by hypoperfused kidneys. In case of massive pulmonary embolism, if the embolism obstructs 50% of the pulmonary artery, it will cause acute right ventricular failure. This will severely reduce venous return to the left ventricle and thus the cardiac output falls drastically to cause severe cardiogenic shock and even sudden death. Cardiac compressive shock is usually caused by pericardial tamponade, tension pneumothorax or by large diaphragmatic hernia. This is a type of cardiogenic shock, in which the heart is compressed from outside leading to failure of its pumping mechanism, though the heart itself is normal. Such type of shock may occur in cases of severe septicaemia, cholangitis, peritonitis or meningitis. In early stages cardiac output increases, but vascular resistance decreases due to dilated cutaneous arteriovenous shunts. In late cases, vascular permeability increases, so that the blood volume decreases leading to hypovolaemia. In further advanced cases the cardiac function is damaged due to toxins liberated by the organisms. Anaphylactic shock is commonly seen after penicillin administration or administration of serum, dextrose, anaesthetics etc. Such shock is usually caused by bronchospasm, laryngeal oedema and respiratory distress which totally lead to hypoxia. This is aggravated by massive vasodilatation which causes hypotension and ultimately shock. It is the haemorrhagic shock which is the most common form in this group and is discussed in details below :— Haemorrhage mostly occurs from the systemic venules and small veins which usually contain about 50% of the total blood volume. This causes decrease of filling of the pulmonary vasculature, which in turn decreases filling of the left atrium and ventricle. Constriction of venules and small veins displaces blood to the right atrium and ventricle. This causes increase of the diastolic pressure of the right ventricle and also its stroke volume. This causes an increase of blood in the pulmonary vasculature and so into the left atrium and ventricle. Both left atrial and left ventricular fillings increase and so increases the left ventricular stroke volume. Adrenergic discharge constricts sphincters in the splanchnic viscera, kidneys and the skin. This selective vasoconstriction improves filling of the right heart and increases cardiac output. So adrenergic discharge takes away a portion of the blood flow from the splanchnic viscera, kidneys and skin and diverts it to the heart and brain. Spontaneous deep breathing sucks blood from extrathoracic sites to the heart and lungs. It must be remembered that both adrenergic discharge and hyperventilation occur within one minute of blood loss. It selectively constricts the vasculature of the splanchnic organs, kidneys and the skin. After haemorrhage another vasoactive hormone, Vasopressin is released due to stimulus from the baroreceptors such as those situated in the carotid bodies and aortic arch caused by hypotension. Vasopressin acts as a systemic vasoconstrictor thus diverting blood to the brain and heart and increases cardiac output. Epinephrine is also vasoactive hormone which is released from the adrenal medulla as a consequence of discharge of the adrenergic nervous system. Release of vasoactive hormones usually takes place after 1 to 2 minutes of haemorrhage. This leads to influx of water, sodium and chloride from the interstitial tissue space into the capillaries. Both these cause hyperosmolarity of the extracellular tissue which draws water out of the cells. Interstitial pressure increases, which forces water, sodium and chloride across the capillary endothelium into the vascular space. Aldosterone is concerned with resorption of sodium from the glomerular ultrafiltrate into the vascular space.

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He now gradually slides his fingers downwards along the line of the humerus on both sides buy generic deltasone 10mg on line. Local bony tenderness and bony irregularity at the surgical neck of the humerus suggest fracture neck of the humerus cheap deltasone 20 mg fast delivery. Similarly if the surgeon goes down to palpate the shaft of the humerus generic 40mg deltasone otc, he may exclude the fracture at this site by absence of local bony tenderness and bony irregularity best deltasone 20mg. It must be remembered that in an unbroken bone the medial epicondyle shows the direction of the head of the humerus, whereas the lateral epicondyle shows the direction of the greater tuberosity. If this relation is disturbed, one must suspect the possibility of fracture either at the neck of humerus or at the shaft. In case of dislocation of shoulder one can try to rotate the arm by rotating the flexed elbow. If there is no transmitted rotation of the head of the humerus and a crepitus and pain are felt at the neck of the humerus, the diagnosis of fracture-dislocation is established. Marked tenderness just below the acromion process indicates fracture of the greater tuberosity or rupture of the supraspinatus tendon. The vertebral border of the scapula and the inferior angle though covered by muscles can be easily palpated. The axillary border of the scapula is more difficult to palpate, yet localized bony tenderness and swelling on this border which suggest fracture of the scapula can be elicited. The coracoid process is situated Vi inch below the clavicle at its junction between the medial 2/3rd and lateral l/3rd. This process can be felt easily though it remains under cover of the medial margin of the deltoid. Probably the most difficult fracture of scapula so far as the diagnosis is concerned is the fracture of the neck of the scapula. It is often confused with the fracture of the upper end of the humerus as diffuse swelling in the shoulder region is the common finding. Drooping of the shoulder with tenderness and crepitus by axial pressure upward through the flexed elbow remain the diagnostic feature of the fracture neck of the scapula. Very careful palpation of the upper end of the humerus will reveal no tenderness, whereas palpation medial to the glenoid cavity will elicit tenderness. In acromio-clavicular dislocation the acromial end the length of the arm from the angle of of the clavicle becomes prominent and comes closure to the the acromion to the lateral epicondyle greater tuberosity of the humerus. The former point is the tip of the coracoid process and the acromial end of the slightly posteriorly placed in comparison clavicle becomes increased. The angle of the acromion is the point where the spine of the scapula bends forward to become the acromion process. So in subcoracoid dislocation of the shoulder as well as in fracture neck of the humerus and shaft of the humerus the length of the arm will be shortened. In subglenoid dislocation of the shoulder and fracture neck of the scapula the length of the arm will be longer. It must be remembered that any damage to the upper epi­ physis of the humerus will shorten the length of the arm. But this measurement will also be increased in conditions like fracture of the upper end of the humerus and fracture neck of the scapula. This is because of the presence of the greater tuberosity of the humerus which pushes the ruler away from the acromion process. But this becomes possible in dislocation of the shoulder where the greater tuberosity of the humerus is displaced medially. After reduction of the dislocation in a muscular patient this test helps to be definite about the reduction and this position is maintained during the post-reduction period. This nerve besides supplying the deltoid muscle gives off a cutaneous twig which supplies the skin over the lower part of the deltoid muscle. Any injury at this region will limit the abduction of the shoulder joint by itself and it is of no use asking the patient to abduct the shoulder to test for the integrity of the axillary nerve. For this it is better to test the sensation of the skin supplied by the cutaneous branch of the axillary nerve. Even when the diagnosis is almost certain by clinical examination, X-ray is essential to know more precisely the line of fracture, the type of displacement (e. In abduction type of fracture of the neck of the humerus the shaft is abducted in relation to the humeral head that means the outer half of the fracture is impacted. In dislocation of the shoulder the position of the head of the humerus indicates the type of dislocation. When the diagnosis is in doubt due to excessive swelling around the shoulder region, X-ray becomes the mode of diagnosis. The fracture usually takes place at the junction of the middle third and the outer third of the clavicle. Very often the lateral fragment is pulled down by the weight of the arm and the medial fragment is displaced upward by the pull of the sternomastoid muscle. On examination there is an obvious swelling by the displaced medial fragment and localized tenderness at the fracture site. On examination an abnormal swelling becomes obvious at the inner end of the clavicle with localized tenderness at that region. It must be remembered that rupture of the acromio­ clavicular ligaments will only cause subluxation of the acromio-clavicular joint. For complete dislocation to occur there must be rupture of the conoid and the trapezoid ligaments which constitute the coraco-clavicular ligament. Swelling, bruising, local tenderness and bony irregularity are elicited on examination. A careful examination and radiological investigation will confirm the exact site of fracture. Forced extension along with lateral rotation will drive the head of the humerus forward tearing the capsule or avulsing the glenoid labrum. Nearly always the head takes the position just below the coracoid process and attains the name of subcoracoid dislocation. Rarely the head may lie below the glenoid cavity when it is called the subglenoid dislocation. It may so happen that the whole dislocation process occurs in the abducted position of the arm and the acromion process levers the head downwards to attain a position called luxatio in erecta. Posterior dislocation is a very rare occurrence and caused by a forced internal rotation on the abducted arm. Very occasionally is the dislocation complete and what is more common is subluxation with fracture of the head of the humerus. The round contour of the shoulder joint is lost and it becomes flattened due to absence of the greater tuberosity at its normal position. On careful inspection one may find a bulge at the deltopectoral groove caused by the head of the humerus which is easily confirmed by rotating the arm with flexed elbow. The patient would not be able to touch the opposite shoulder with the hand of the affected side. When the anterior capsule is stripped from the anterior margin of the glenoid rim but attached to the neck of the scapula, there remains a chance of recurrent dislocation as the head of the humerus always remains within the capsule but outside the glenoid cavity. This condition may also occur when the glenoid labrum is detached along with the capsule and when there is a bony defect gouged out at the postero­ lateral aspect of the humeral head. The surgical neck breaks and the upward thrust may shear off the greater tuberosity. A direct injury on the point of the shoulder may cause fracture at the anatomical neck of the humerus. It may occur in association with dislocation of the shoulder and fracture neck of the humerus. A young child with swollen flexed elbow supported by his other hand is probably a case of supracondylar fracture of humerus. Attitude of the elbow joint has to be observed from in front, behind and from side. In majority cases of injury to the elbow the joint is held in the position of flexion, (ii) Carrying angle.

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The part extending from-the mental foramen to the symphysis menti is by cartilaginous ossification and the rest is membraneous bone deltasone 40 mg visa. Muscular elements develop into (i) tensor tympani order deltasone 10 mg overnight delivery, (ii) tensor veli palatini and muscles of mastication which include (iii) the masseter buy cheap deltasone 5 mg line, (iv) temporalis muscle buy 10mg deltasone visa, (v) medial and lateral pterygoids, (vi) mylohyoid and (vii) anterior belly of the digastric. According to some the maxillary artery may be the remnant of the first aortic arch. Thereafter it forms as it passes ventrally (ii) styloid process, (iii) stylohyoid ligament, (iv) the lesser cornu and (v) the upper part of the body of the hyoid bone. The ventral portion chondrifies and persists as the (i) greater comu of the hyoid bone and (ii) lower part of whole of the body of the hyoid. The external carotid artery appears as a sprout from the middle of the third arch and grows headwards. The ventral portion of the arch upto the sprout forms the common carotid artery and the dorsal portion from the sprout forms the internal carotid artery. The dorsal part disappears on the right side, while it persists on the left side as ductus arteriosus communicating with the arch of the aorta. Ductus arteriosus after birth becomcs obliterated and forms ligamentum arteriosum. The second arch gradually overlaps over the third and fourth arches at the end of the fifth week. The ridge produced by this arch grows downwards and meets caudally a smaller bridge termed the epipericardial ridge just above the pericardium. A small depression is formed which lies superficial to the third and fourth arches and deep to the second arch. So in fact, third and fourth arches do not take part in forming the ectodermal covering of the neck. From the ridge formed by the second branchial arch develops the stemomastoid and the trapezius muscles. If the sec­ ond arch fails to fuse with the 5th arch or epiper­ icardial ridge, a fistula develops and it connects the precervical sinus. If it arises from the internal branchial furrow the epithelium may be columnar and ciliated. The striking feature of this cyst is that its wall contains large amount of lymphoid tissue. The contents are viscid, mucoid, cheesy material and cholesterol crystals in large numbers. If infected the swelling may be painful and it becomes difficult to differentiate from acute lymphadenitis, chronic lymphadenitis or tuberculous lymphadenitis and cold abscess. The stemomastoid muscle develops from the migrated myotome in the ridge of the second branchial arch which covers the pre- cervical sinus. The branchial cyst develops from the precervical sinus, so it will always be deep to the stemomastoid muscle. The overlying skin looks normal, though if infected, may be red and angry looking. Fluctuation test will be positive, but is difficult to elicit when the cyst is small and the stemomastoid muscle is thick. Some amount of the content may be aspirated before dissection so that the wall of the cyst may be grasped with suitable forceps without injuring it. Sometimes it extends between the origins of the internal and external carotid arteries upto the pharyngeal wall. Hypoglossal and glossopharyngeal nerves lie deep to the cyst and they should be protected. It is usually situated in the upper or middle thirds of the neck and often continues to discharge. Congenital branchial fistula is often a branchial sinus without any communication inside. From the development it is clear that branchial fistula represents a persistent second branchial cleft which covers the third and fourth branchial arch. So usually there should not be any internal opening and in the true sense it is a ‘branchial sinus’. The membrane which intervenes between the second branchial cleft and the second branchial pouch which forms the supratonsillar fossa at times may disappear or perforate by injudicious use of probe and then a branchial sinus becomes a branchial fistula and opens in the anterior aspect of the posterior pillar of the fauces, just behind the tonsil. The fistula then passes through the bifurcation of the common carotid artery being superficial to the internal carotid artery and deep to the external carotid artery. As the fistula arises from the second branchial cleft being covered by the second branchial arch superficially, so all the structures derived from the second arch will be superficial to this fistula and the structures developed from the third branchial arch will lie deep to this fistula. Internal carotid artery is derived from the third arch while the external carotid artery sprouts out of the third arch and immediately becomes superficial, so the fistula traverses between these two arteries. The fistula passes deep to the posterioi belly of the digastric and the stylohyoid muscle. It crosses superficial to the internal jugular vein and the hypoglossal nerve, the glossopharyngeal nerve and the stylopharyngeus muscle (derivatives of 3rd arch). It then pierces the superior constrictor muscle and opens on the posterior pillar of the fauces behind the tonsil. The stratified squamous epithelium or pseudostratified ciliated columnar epithelium forms the epithelium lining. According to a few pathologists columnar ciliated epithelium forms the epithelium lining. But since this fistula is remnant of branchial cleft there is more possibility that the lining will be stratified squamous variety. Due to the presence of lymphoid tissue recurrent inflammation is common and not infrequently the epithelial lining is replaced by chronically inflamed granulation tissue. It often discharges from the external opening either mucoid or mucopurulent fluid. As the condition is not much troublesome patients often come to the clinician late. It is nearly always situated in the lower third of the neck near the anterior border of the stemomastoid muscle (cf. A sinogram may be made by injecting radio-opaque dye into the fistulous track to know the upper limit of the fistula. Gentle traction to the fistula track will facilitate identification of the fistula and its dissection upwards. A second incision may be required above the upper border of the thyroid cartilage transversely placed along the Langer’s line. The upper part of the track is dissected through this incision upto the pharyngeal wall. During dissection one must be careful, as many important nerves and blood vessels, which have been discussed earlier, are around. As a matter of fact a clinical diagnosis of branchiogenic carcinoma is rarely justified until and unless one very clearly excludes primary growth in the mouth, tongue, pharynx, larynx and external auditory meatus. Again at times a primary carcinoma of the mouth or pharynx may remain silent for months, the only evidence of its presence being a deep-seated cervical lymph node. This carcinoma is commoner in males and is situated deep in the neck near the bifurcation of the common carotid artery. It infiltrates the surrounding structures and metastasises to the regional lymph nodes. Microscopi­ cally, the tumour consists of squamous or transitional cells arranged in masses, in the centre of which cavities may appear due to necrosis. One pair in the neck called jugular lymph sacs develop near the origin of the internal jugular vein. One at the retroperitoneal tissue and another lymph sac is called cy sterna chyli. Another pair develops near the inguinal region below the bifurcation of the common iliac vein. The jugular lymph sac is first to appear at the junction of the subclavian vein with the anterior cardinal vein which ultimately forms the jugular vein. Sequestration of a portion of the jugular sac from the lymphatic system which fails to join the regular lymphatic system accounts for the appearance of cystic hygroma. Cystic hygroma may infiltrate into the muscle planes and these extensions may grow deep. The swelling gradually extends upwards towards the ear or downwards towards the axilla. The swelling may attain such a huge size that it becomes difficult to know which is the actual site of origin.

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