Jason W. Custer, MD

• Fellow
• Department of Pediatric Critical Care
• Johns Hopkins University
• Baltimore, Maryland

Many patients with hematemesis and most patients with hematochezia (bloody stools) have a nonsurgical condition blood pressure z score calculator order innopran xl 40mg fast delivery. In breastfed infants hypertension 140 80 buy innopran xl 80 mg on line, either microscopic or macroscopic blood noted several days after birth in either emesis or stool may be due to swallowed blood during breastfeeding in setting of cracked maternal nipples heart attack medication buy innopran xl 80 mg without a prescription. Necrotizing enterocolitis (most frequent cause of hematemesis and bloody stool in premature infants; see Chap prehypertension stage 1 stage 2 innopran xl 80mg line. Hepatosplenomegaly: may be confused with other masses; requires medical evaluation 3 blood pressure 360 buy cheap innopran xl 80mg online. Compromised pulmonary capacity due to diaphragmatic elevation secondary to abdominal distension iv pulse pressure 2012 discount 40mg innopran xl overnight delivery. Reflux of gastric contents up the distal esophagus into the lungs through the fistula Surgery 813 b. The diagnosis is suggested by a history of frequent pneumonias or respiratory distress temporally related to meals. Air is then injected into the catheter while listening (for lack of air) over the stomach. The diagnosis is confirmed by x-ray studies showing the catheter coiled in the upper esophageal pouch. Plain x-ray films may demonstrate a distended blind upper esophageal pouch filled with air that is unable to progress into the stomach. This disorder can often be demonstrated with administration of nonionic water-soluble contrast medium (Omnipaque) during cinefluoroscopy. The definitive examination is combined fiberoptic bronchoscopy and esophagoscopy with passage of a fine balloon catheter from the trachea into the esophagus. Approximately 20% of these babies are premature (five times the normal incidence), and another 20% are small for gestational age (eight times the normal incidence). A multiple end-hole suction catheter (Replogle) should be placed in the proximal pouch and put to continuous suction immediately after the diagnosis is made. The head of the bed should be elevated 30 degrees to diminish reflux of gastric contents into the fistula and aspiration of oral secretions that may accumulate in the proximal esophageal pouch. If possible, mechanical ventilation of these babies should be avoided until the fistula is controlled because the positive pressure may cause severe abdominal distension compromising respiratory function. Guidelines for intubation are the same as for other types of respiratory distress (see Chap. The endotracheal tube should be advanced to just above the carina in the hopes of obstructing airflow through the fistula. As soon as the infant can tolerate further surgery, the fistula is divided; and, if possible, the proximal and distal ends of the esophagus are anastamosed primarily. These babies need careful nursing care to prevent aspiration and gastrostomy with G-tube feedings to allow growth until repair is possible. If the infant has cardiac disease that requires surgery, it is usually best to repair the fistula first. We have developed a referral center for such patients who are treated with innovative esophageal growth induction techniques that can allow for primary repairs, thereby avoiding the need for gastric, colonic, or jejunal interposition. The most common site is the left hemithorax, with the defect in the diaphragm being posterior (foramen of Bochdalek) in 70% of infants. Fifty percent of these hernias are associated with other malformations, especially cardiac, neural tube, intestinal, skeletal, and renal defects. Small hernias, right-sided hernias, sac-type hernias, and substernal hernias of Morgagni may have a more subtle presentation, manifested as feeding problems and mild respiratory distress. Diagnosis earlier in gestation may correlate with a poorer prognosis due to severity of condition. The prognostic advantage of prenatal diagnosis is that it generally leads to delivery in a center, equipped to optimize chances for survival. If delivery before term is likely, fetal lung maturity should be assessed to evaluate the need for maternal betamethasone therapy (see Chap. Presence of liver in the thorax correlates with increased Surgery 815 severity and poorer prognosis. Because of the possibility of marked cardiothymic shift, a radiopaque marker should be placed on one side of the chest to aid interpretation of the x-ray film. Diaphragmatic eventration, congenital cystic adenomatoid malformation, pulmonary sequestration, and bronchogenic cyst. Maternal laparotomy is performed, with exposure of the uterus, which should be extremely hypotonic because of the anesthesia. Bleeding is minimized by using a special device to open the uterus that simultaneously cuts a full-thickness uterine incision and places hemostatic clips along the incision. A pulse oximeter probe is placed on the fetal hand to permit direct monitoring of heart rate and oxygen saturation, with the oxygen saturation maintained at fetal levels of approximately 60%. If the saturation gets too high, the umbilical vessels will constrict and the umbilical blood supply will diminish. All infants should be intubated immediately after delivery if the diagnosis has been made antenatally or at the time of postnatal diagnosis. Immediately after intubation, a large sump nasogastric tube should be inserted and attached to continuous suction. Care must be taken with assisted ventilation to keep inspiratory pressures low to avoid damage or rupture of the contralateral lung. Peripheral venous and arterial lines are preferable, as umbilical lines may need to be removed during surgery. However, if umbilical lines are the only practical access, these should be placed initially. Preoperative management is focused on avoiding barotrauma and minimizing pulmonary hypertension. That said, permissive hypercapnia is the preferred respiratory approach, although the mode of ventilation remains controversial, including the role for high-frequency ventilation. Surgical repair is through either the abdomen or the chest, with reduction of intestine into the abdominal cavity. Repair of the defect itself is relatively straightforward; the underlying pulmonary hypoplasia and pulmonary hypertension are largely responsible for overall mortality (see Chap. Factors associated with better prognosis are herniation of bowel into chest after 2nd trimester, absence of liver herniation, and absence of coexisting anomalies, especially cardiac. In addition, the later the onset of postnatal symptoms, the higher the survival rate. Bilateral atresia presents in the delivery room as respiratory distress that resolves with crying. Definitive therapy includes opening a hole through the bony plate, which can be accomplished with a laser in some settings. Robin anomaly (Pierre Robin syndrome) consists of a hypoplastic mandible associated with a secondary, U-shaped midline cleft palate. Prone positioning or forcibly pulling the tongue forward will relieve the obstruction. These infants often improve after placement of a nasopharyngeal or endotracheal tube. If the infant can be supported for a few days, he or she will sometimes adapt, and aggressive procedures can be avoided. In some cases, a lip tongue adhesion or mandibular distraction can avoid the need for tracheostomy or enable earlier decannulation. The diagnosis is made by instillation of contrast material into the esophagus and is confirmed by bronchoscopy. Perforation of the web by a stiff endotracheal tube or bronchoscopy instrument may be lifesaving. Surgery 817 Diagnosis is by use of contrast material in the esophagus and by endoscopy. Congenital lobar emphysema may be due to a malformation, a cyst in the bronchus, or a mucous or meconium plug in the bronchus. These lesions cause air trapping, compression of surrounding structures, and respiratory distress. After consultation with a surgeon, selective intubation of the opposite bronchus may be attempted in an effort to decompress the emphysematous lobe if overinflation is thought to be the cause. It should generally be viewed as a temporizing therapy and should not be employed for more than a few hours. Many infants will not tolerate this procedure due to both overdistension of the ventilated lung and profound V:Q mismatch; therefore, it must be carefully considered and monitored. Rarely, selective intubation is successful and the lobar emphysema does not recur. Much more commonly, even if the selective intubation is initially helpful, the baby goes on to develop recurrence and progression of the emphysema and further respiratory compromise. Occasionally, selective suctioning of the bronchus on the side of the emphysema may remove obstructing mucus or meconium. If the baby is symptomatic and conservative measures fail, bronchoscopy should be performed to remove any obstructing material or rupture a bronchogenic cyst. If this procedure fails, surgical resection of the involved lobe should be considered. All patients with suspected intestinal obstruction should have a nasogastric sump catheter placed to continuous suction without delay. Intrinsic types include atresia, stenosis, hypertrophic pyloric stenosis, cysts within the lumen of the bowel, and imperforate anus. Extrinsic forms of congenital mechanical obstruction include congenital peritoneal bands with or without malrotation, annular pancreas, duplications of the intestine, aberrant vessels (usually the mesenteric artery or preduodenal portal vein), hydrometrocolpos, and obstructing bands (persistent omphalomesenteric duct). Functional intestinal obstruction constitutes the major cause of intestinal obstruction seen in the neonatal unit. Defective innervation (Hirschsprung disease) or other intrinsic defects in the bowel wall 3. Pyloric stenosis typically presents with nonbilious vomiting after the age of 2 to 3 weeks, but it has been reported in the first week of life. Radiographic examination will show a large stomach with little or no gas below the duodenum. The infant may pass meconium in the first 24 hours of life; then bowel movements cease. The diagnosis is suggested if aspiration of the stomach yields 30 mL of gastric contents before feeding. A plain radiograph of the abdomen will show air in the stomach and upper part of the abdomen ("double bubble") with no air in the small or large bowel. Unlike most other etiologies of obstruction in which flat and upright x-ray films will demonstrate fluid levels, in cases of nonperforated meconium ileus, the distended bowel may be granular in appearance or may show tiny bubbles mixed with meconium. If the results are negative or equivocal or if the baby weighs 2 kg and is older than 2 weeks ideally (but certainly older than 3 days), a sweat test should be performed. Sweat tests on babies who are younger or smaller risk both false-positive results due to the high NaCl content of the sweat of newborns and false-negative or uninterpretable results when an adequate volume of sweat cannot be obtained. Decompression with continuous nasogastric suction will minimize further distention. Meglumine diatrizoate (Gastrografin) or diatrizoate sodium (Hypaque) can be used in an adequately hydrated infant. Because these contrast agents are hypertonic, the baby should start the procedure well hydrated, and careful attention should be paid to fluid balance after the procedure. If the diagnosis is certain and the neonate is stable, repeat therapeutic enemas may be administered in an effort to relieve the impaction. Surgical therapy is required if the contrast enema fails to relieve the obstruction. Infants with imperforate anus may pass meconium if a rectovaginal or rectourinary fistula exists. The presence or absence of a visible fistula at the perineum is the critical distinction in the diagnosis and management of imperforate anus. This fistula may be dilated to allow passage of meconium to temporarily relieve intestinal obstruction. When the infant is beyond the newborn period, the imperforate anus can generally be primarily repaired. The presence of meconium particles in the urine is diagnostic of a rectovesicular fistula. A cystogram may show a fistula and document the level of the distal rectum, which can also be defined by ultrasonography. A temporary colostomy may be necessary in neonates with an imperforate anus without a perineal fistula. Primary repair of these infants without a colostomy is now being performed at some institutions. If this condition develops during fetal life, it may cause the appearance of a large midabdominal calcific shadow on x-ray examination; this results from calcification of meconium in the segment of necrotic bowel. After birth, there is a sudden onset of bilious vomiting in an infant who has passed some normal stools. Malrotation, as the cause of intestinal obstruction, is a surgical emergency because intestinal viability is at stake. A radiograph of the abdomen will often show a dilated small bowel, although a normal radiograph does not rule out malrotation, which can be intermittent. If a malrotation is present, barium enema may show failure of barium to pass beyond the transverse colon or may show the cecum in an abnormal position. Annular pancreas may be nonobstructing but associated with duodenal atresia or stenosis. In this rare condition, a membrane across the vagina prevents fluid drainage and the consequent accumulation causes distension of the uterus and vagina. Accumulated secretions in the uterus may cause intestinal obstruction by bowel compression.

Syndromes

• Bluish lips
• Numbness or tingling occur just after a head, neck, or back injury
• Dizziness and headaches
• Feeling weak or tired
• CT scan of the lungs
• In most cases, the doctor will use medicine to close off the opening. If this does not work, then other techniques are used to close the opening.
• Some drugs
• Practice safer sex.

Vascular injuries arrhythmia 1 innopran xl 80 mg overnight delivery, unstable fractures arrhythmia alliance purchase 80 mg innopran xl with amex, contaminated soft tissues and tendon divisions should be dealt with before the nerve lesion pulse pressure 57 generic innopran xl 40mg amex. The incision will be long blood pressure medication that doesn't cause dizziness 80mg innopran xl free shipping, as the nerve must be widely exposed above and below the lesion before the lesion itself is repaired blood pressure question purchase innopran xl 40 mg free shipping. If microsurgical equipment and expertise are not available blood pressure of 90 60 proven 40mg innopran xl, then the nerve lesion should be identified and the wound closed pending transferral to an appropriate facility. A clean cut nerve is sutured without further preparation; a ragged cut may need paring of the stumps with a sharp blade, but this must be kept to a minimum. The stumps are anatomically orientated and fine (10/0) sutures are inserted in the epineurium. Sufficient relaxation of the tissues to permit tension-free repair can usually be obtained by positioning the nearby joints or by mobilizing and re-routing the nerve. These injuries are best dealt with in specialized centres, where primary grafting or nerve transfer can be carried out. If a tourniquet is used it should be a pneumatic one; it must be released and bleeding stopped before the wound is closed. The limb is splinted in a position to ensure minimal tension on the nerve; if flexion needs to be excessive, a graft is required. The options must be carefully weighed: if the patient has adapted to the functional loss, if it is a high lesion and re-innervation Primary repair A divided nerve is best repaired as soon as this can be done safely. Primary suture at the time of wound toilet has considerable advantages: the nerve ends 274 is unlikely within the critical 2-year period, or if there is a pure motor loss which can be treated by tendon transfers, it may be best to leave well alone. Excessive scarring and intractable joint stiffness may, likewise, make nerve repair questionable; yet in the hand it is still worthwhile simply to regain protective sensation. The lesion is exposed, working from normal tissue above and below towards the scarred area. When the nerve is in continuity it is difficult to know whether resection is necessary or not. The stumps may be brought together by gently mobilizing the proximal and distal segments, by flexing nearby joints to relax the soft tissues, or (in the case of the ulnar nerve) by transposing the nerve trunk to the flexor aspect of the elbow. It is also possible to use free vascularized grafts for certain brachial plexus lesions. Nerve transfer In root avulsions of the upper brachial plexus, too proximal for direct repair, nerve transfer can be used. The spinal accessory nerve can be transferred to the suprascapular nerve, and intercostal nerves can be transferred to the musculocutaneous nerve. If biceps has failed because too much time has passed since the injury, an entire muscle (gracilis or latissimus dorsi) can be transferred as a free flap, attached between elbow and shoulder and then innervated by joining Nerve guides It is now apparent that nerve gaps can regenerate through a tube which excludes the surrounding tissue from each end. The tubes can be autogenous vein, freeze-dried muscle, silicone or metal; soluble guides (flexible at body temperature) which dissolve over weeks or months are also used. This technology offers a simple way of avoiding a nerve graft yet achieving results which are at least as good in both digital nerves and probably in main trunks. The donor muscle should be: expendable powerful enough an agonist or synergist the recipient site should: be stable have mobile joints and supple tissues the transferred tendon should be: routed subcutaneously placed in a straight line of pull capable of firm fixation the patient should be: motivated able to comprehend and attend hand therapy Nerve grafting Free autogenous nerve grafts can be used to bridge gaps too large for direct suture. The graft should be long enough to lie without any tension, and it should be routed through a well-vascularized bed. It is crucial that the motor and sensory fascicles are appropriately connected by the graft. Careful inspection of the fascicular alignment, structure and vascular markings is often helpful. The joints should be moved through their full range twice daily to prevent stiffness and minimize the work required of muscles when they recover. Associated lesions Damage to vessels, tendons and other structures makes it more difficult to obtain recovery of a useful limb even if the nerve itself recovers. Surgical techniques Skill, experience and suitable facilities are needed to treat nerve injuries. If these are lacking, it is wiser to perform the essential wound toilet and then transfer the patient to a specialized centre. This is most likely when there is a proximal injury in a nerve supplying distal muscles. Type of nerve Purely motor or purely sensory nerves recover better than mixed nerves, because there is less likelihood of axonal confusion. Dorsal scapular nerve C5 C6 Suprascapular nerve C7 T1 Radial nerve T2 Long thoracic nerve Axillary nerve Lateral and medial pectoral nerves Musculocutaneous nerve Medial cutaneous nerve of arm Medial cutaneous nerve of forearm Median nerve Ulnar nerve 276 11. Traction injuries are generally classed as supraclavicular (65 per cent), infraclavicular (25 per cent) and combined (10 per cent). Supraclavicular lesions typically occur in motorcycle accidents: as the cyclist collides with the ground or another vehicle his neck and shoulder are wrenched apart. In the most severe injuries the arm is practically avulsed from the trunk, with rupture of the subclavian artery. Infraclavicular lesions are usually associated with fractures or dislocations of the shoulder; in about a quarter of cases the axillary artery also is torn. Fractures of the clavicle rarely damage the plexus and then only if caused by a direct blow. The injury may affect any level, or several levels within the plexus, often involving a mixture of nerve root(s), trunk(s) and nerve(s). An important distinction is made between preganglionic and postganglionic lesions. Rupture of a nerve root distal to the ganglion, or of a trunk or peripheral nerve, is a postganglionic lesion, which is surgically reparable and potentially capable of recovery. Lesions in continuity, from first to fourth degree, generally have a better prognosis than complete ruptures. Mild lesions (neurapraxia) are fairly common and may be caused by comparatively trivial trauma such as sudden compression by a tight harness or motor vehicle seatbelt; these recover spontaneously but mild residual symptoms may prove a nuisance for many months. By examining systematically for each component of the brachial plexus (roots, trunks, divisions, cords and branches) the exact site of the lesion may be identified. For instance, preservation of the dorsal scapular nerve (rhomboids), long thoracic nerve (serratus anterior) and suprascapular nerve (supraspinatus), but loss of musculocutaneous nerve function (biceps), radial nerve (triceps) and axillary nerve (deltoid) suggest a lateral and posterior cord injury. Preganglionic lesions (root avulsions) are irreparable; postganglionic lesions may either recover (axonotmesis) or may be amenable to repair. Intradermal injection of histamine usually causes a triple response in the surrounding skin (central capillary dilatation, a wheal and a surrounding flare). If the flare reaction persists in an anaesthetic area of skin, the lesion must be proximal to the posterior root ganglion, i. With a postganglionic lesion the test will be negative because nerve continuity between the skin and the dorsal root ganglion is interrupted. If there is sensory conduction from an anaesthetic dermatome, this suggests a preganglionic lesion Clinical features Brachial plexus injuries are often overshadowed by other, life-threatening trauma which needs immediate attention. Associated injuries, such as rupture of the subclavian or axillary artery, should be sought and attended to , otherwise a poor outcome is inevitable. Detailed clinical examination is directed at answering specific questions: What is the level of the lesion As long as recovery proceeds at the expected rate, watchful conservation is the byword. If recovery falters, or if special investigations show that it is more than a second degree lesion, then the patient should be referred to a special centre for surgical exploration of the brachial plexus and nerve repair, grafting or nerve transfer procedures. The sooner this decision is made, the better: during the early days operative exposure is easier and the response to repair more reliable. There are few donor axons available to neurotize the upper levels (shoulder and elbow function) and no recovery will take place in the hand. The implication is that all efforts for nerve repair or nerve transfer are directed towards lesions involving C5 and 6. The objectives are to regain shoulder abduction, elbow flexion, wrist extension, finger flexion, and sensibility over the lateral (radial) side of the hand. If C5 and C6 are avulsed, then the spinal accessory nerve can be transferred to the suprascapular nerve; or two or three intercostal nerves can be transferred to the musculocutaneous nerve. C5) then this should be grafted on to the lateral cord which will supply elbow flexion, finger flexion and sensation over the radial side of the hand. These procedures bypass the suprascapular nerve which is joined to the spinal accessory nerve. With complete preganglionic loss, the contralateral C7 root can be extended across the chest with autologous graft and then used as an axon source into the plexus. This test becomes reliable only after a few weeks, when wallerian degeneration in a postganglionic lesion will block nerve conduction. The history is informative: the mechanism of injury and the impact velocity may suggest either a mild (first or second degree) or a severe (fourth or fifth degree) injury. With the former a period of observation is justified; a first or second degree lesion may show signs of recovery by 6 or 8 weeks. Since there may be different degrees of injury within the plexus, some muscles may recover while others fail to do so. Management the patient is likely to be admitted to a general unit where fractures and other injuries will be given priority. Emergency surgery is required for brachial plexus lesions associated with penetrating wounds, vascular injury or severe (high energy) soft-tissue damage whether open or closed; clean cut nerves should be repaired or grafted. All other closed injuries are left until detailed examination and special investigations have been completed. Patients with root avulsion or severe, mutilating injuries of the limb will be unsuitable for nerve surgery, at least until the prognosis for limb function becomes clear. The nerve supply to these muscles must remain intact, so they are suitable only for certain patterns of injury. Further examination a day or two later will define the type of brachial plexus injury. The abductors and external rotators of the shoulder and the supinators are paralysed. Shoulder arthrodesis Arthrodesis is usually reserved for an unstable or painful shoulder, perhaps after failure of re-innervation of the supraspinatus. The baby lies with the arm supinated and the elbow flexed; there is loss of intrinsic muscle power in the hand. X-rays should be obtained to exclude fractures of the shoulder or clavicle (which are not uncommon and which can be mistaken for obstetrical palsy). Paralysis may recover completely Many (perhaps most) of the upper root lesions recover spontaneously. If the serratus anterior is paralysed, the scapula cannot be held firmly against the rib-cage. Paralysis may remain unaltered this is more likely with loads on the shoulder, and even viral illnesses or toxoid injections. Unless the roots are avulsed, it may be possible to excise the scar and bridge the gap with free sural nerve grafts; if the roots are avulsed, nerve transfer may give a worthwhile result. This is highly demanding surgery which should be undertaken only in specialized centres. If diligent physiotherapy does not prevent this, then a subscapularis release will be needed, sometimes supplemented by a tendon transfer. In older children, the deformity can be treated by rotation osteotomy of the humerus. Clinical features Paralysis of serratus anterior is the commonest cause of winging of the scapula. Examination shows little abnormality until the arm is elevated in flexion or abduction. The classic test for winging is to have the patient pushing forwards against the wall or thrusting the shoulder forwards against resistance. Treatment Except after direct injury or division, the nerve usually recovers spontaneously, though this may take a year or longer. Persistent winging of the scapula occasionally requires operative stabilization by transferring pectoralis minor or major to the lower part of the scapula. Contrary to general belief, the nerve appears also to have sensory functions, including pain sensibility. Because of its superficial course, it is easily injured in stab wounds and operations in the posterior triangle of the neck. There is usually wasting of the supraspinatus and infraspinatus, with diminished power of abduction and external rotation. Peripheral nerve disorders Treatment this is usually an axonotmesis which clears up spontaneously after 3 months. In the absence of trauma one might suspect a nerve entrapment syndrome, and decompression by division of the suprascapular ligament often brings improvement. The operative approach is through a posterior incision above and parallel to the spine of the scapula. Examination reveals asymmetry or drooping of the shoulder, reduced ability to hitch or hunch the shoulder and weakness on abduction of the arm; typically there is mild winging of the scapula on attempting active abduction against resistance; unlike the deformity in serratus anterior palsy, this disappears on flexion or forward thrusting of the shoulder. Often the true nature of the problem is not appreciated and diagnosis is delayed for weeks or months. It emerges behind the humerus, deep to the deltoid; after supplying the teres minor, it divides into a medial branch which supplies the posterior part of the deltoid and a patch of skin over the muscle and an Treatment Stab injuries and surgical injuries should be explored immediately and the nerve repaired.

A single motor neuron may supply anything from 10 to several thousand muscle fibres heart attack kid discount 80mg innopran xl with amex, the ratio depending on the degree of dexterity demanded of the particular muscle (the smaller the ratio blood pressure er innopran xl 40 mg overnight delivery, the finer the movement) pulse pressure from blood pressure generic innopran xl 40 mg otc. Similarly pulse pressure 93 generic 80mg innopran xl otc, the peripheral branches of each sensory neuron may serve anything from a single muscle spindle to a comparatively large patch of skin; here again blood pressure 200 100 purchase innopran xl 80mg visa, the fewer the end receptors served the greater the degree of discrimination percentil 95 arteria uterina buy innopran xl 80mg cheap. The signal, or action potential, carried by motor neurons is transmitted to the muscle fibres by the release of a chemical transmitter, acetylcholine, at the terminal bouton of the nerve. Sensory signals are similarly conveyed to the dorsal root ganglia and from there up the ipsilateral column of the spinal cord, through the brain-stem and thalamus, to the opposite (sensory) cortex. Proprioceptive impulses from the muscle spindles and joints bypass this route and are carried to the anterior horn cells as part of a local reflex arc. In the peripheral nerves, all motor axons and the large sensory axons serving touch, pain and proprioception are coated with myelin, a multilayered lipoprotein membrane derived from the accompanying Schwann cells. Nerve impulses leap from node to node at the speed of electricity, much faster than would be the case if these axons were not insulated by the myelin sheaths. Damage to these axons causes unpleasant or bizarre sensations and various sudomotor and vasomotor effects. Outside the Schwann cell membrane the axon is covered by a connective tissue stocking, the endoneurium. The axons that make up a nerve are separated into bundles (fascicles) by fairly dense membranous tissue, the perineurium. In a transected nerve, these fascicles are seen pouting from the cut surface, their perineurial sheaths well defined and strong enough to be grasped by fine instruments during operations for nerve repair. The groups of fascicles that make up a nerve trunk are enclosed in an even thicker connective tissue coat, the epineurium. The nerve is richly supplied by blood vessels that run longitudinally in the epineurium before penetrating the various layers to become the endoneurial capillaries. These fine vessels may be damaged by stretching or rough handling of the nerve; however, they can withstand extensive mobilization of the nerve, making it feasible to repair or replace damaged segments by operative transposition or neurotization. The tiny blood vessels have their own sympathetic nerve supply coming from the parent nerve, and stimulation of these fibres (causing intraneural vasoconstriction) may be important in conditions such as reflex sympathetic dystrophy and other unusual pain syndromes. Damage varies in severity from transient and quickly recoverable loss of function to complete interruption and degeneration. There may be a mixture of types of damage in the various fascicles of a single nerve trunk. Transient ischaemia Acute nerve compression causes numbness and tingling within 15 minutes, loss of pain sensibility after 30 minutes and muscle weakness after 45 minutes. These changes are due to transient endoneurial anoxia and they leave no trace of nerve damage. Axonotmesis this is a more severe form of nerve injury, seen typically after closed fractures and dislocations. There is loss of conduction but the nerve is in continuity and the neural tubes are intact. It is now recognized that severe degrees of damage may be inflicted without actually dividing the nerve. If the injury is more severe, whether the nerve is in continuity or not, recovery will not occur. As in axonotmesis, there is rapid wallerian degeneration, but here the endoneurial tubes are destroyed over a variable segment and scarring thwarts any hope of regenerating axons entering the distal segment and regaining their target organs. Even after surgical repair, many new axons fail to reach the distal segment, and those that do may not find suitable Schwann tubes, or may not reach the correct end-organs in time, or may remain incompletely myelinated. This may explain why peripheral entrapment syndromes are often associated with cervical or lumbar spondylosis. One of the tendrils will find its way into the old endoneurial tube and (d) the axon will slowly regenerate. Increasingly, however, it has been recognized that many cases fall into an area somewhere between axonotmesis and neurotmesis. Therefore, following Sunderland (1978), a more practical classification is offered here. First degree injury this embraces transient ischaemia and neurapraxia, the effects of which are reversible. Second degree injury retrograde, axons disintegrate and are resorbed by phagocytes. This wallerian degeneration (named after the physiologist, Augustus Waller, who described the process in 1851) takes only a few days and is accompanied by marked proliferation of Schwann cells and fibroblasts lining the endoneurial tubes. The denervated target organs (motor end-plates and sensory receptors) gradually atrophy, and if they are not reinnervated within 2 years they will never recover. Axonal regeneration starts within hours of nerve damage, probably encouraged by neurotropic factors produced by Schwann cells distal to the injury. From the proximal stumps grow numerous fine unmyelinated tendrils, many of which find their way into the cell-clogged endoneurial tubes. Axonal degeneration takes place but, because the endoneurium is preserved, regeneration can lead to complete, or near complete, recovery without the need for intervention. The endoneurium is disrupted but the perineurial sheaths are intact and internal damage is limited. The chances of the axons reaching their targets are good, but fibrosis and crossed connections will limit recovery. Recovery is unlikely; the injured segment should be excised and the nerve repaired or grafted. If a nerve injury is present, it is crucial also to look for an accompanying vascular injury. Ask the patient if there is numbness, paraesthesia or muscle weakness in the related area. Despite the fact that there is considerable overlap in sensory boundaries, the area of altered sensibility is usually sufficiently characteristic to provide an anatomical diagnosis. Sudomotor changes may be found in the same topographic areas; the skin feels dry due to lack of sweating. The sensory distribution of peripheral nerves is illustrated in the relevant sections. The smooth barrel of the pen is brushed across the palmar skin: normally there is a sense of slight stickiness, due to the thin layer of surface sweat, but in denervated skin the pen slips along smoothly with no sense of stickiness in the affected area. The neurological examination must be repeated at intervals so as not to miss signs which appear hours after the original injury, or following manipulation or operation. The anaesthetic skin may be smooth and shiny, with evidence of diminished sensibility such as cigarette burns of the thumb in median nerve palsy or foot ulcers with sciatic nerve palsy. Beware of trick movements which give the appearance of motor activity where none exists. More specific assessment is required to answer two questions: How severe was the lesion A low energy injury is likely to have caused a neurapraxia; the patient should be observed and recovery anticipated. A high energy injury is more likely to have caused axonal and endoneurial disruption (Sunderland third and fourth degree) and so recovery is less predictable. An open injury, or a very high energy closed injury, will probably have divided the nerve and early exploration is called for. In axonotmesis, it is positive at the site of injury because of sensitivity of the regenerating axon sprouts. After a delay of a few days or weeks, the Tinel sign will then advance at a rate of about 1 mm each day as the regenerating axons progress along the Schwann-cell tube. If the Tinel sign proceeds very slowly, or if muscle groups do not sequentially recover as expected, then a good recovery is unlikely and here again exploration must be considered. After nerve regeneration or repair, a proportion of proximal sensory axons will fail to reach their appropriate sensory end-organ; they will either have regenerated down the wrong Schwann-cell tube or will be entangled in a neuroma at the site of injury. Therefore, two-point discrimination (measured with a bent paper clip and compared with the opposite normal side) gives an indication of how completely the nerve has recovered. Static two-point discrimination measures slowly adapting sensors (Merkel cells) and moving two-point discrimination measures rapidly adapting sensors (Meissner corpuscles and pacinian corpuscles). They are more useful in nerve-compression syndromes, where individual receptors fail to send impulses centrally; two-point discrimination is preserved because the innervation density is not affected. Fine nylon monofilaments of varying widths are placed perpendicularly on the skin and the size of the lightest perceptible filament is recorded. Locognosia is the ability to localize touch and can be tested with a standardized hand map. The patient is blindfolded and instructed to pick up and identify nine objects as rapidly as possible. Exploration is indicated: (1) if the nerve was seen to be divided and needs to be repaired; (2) if the type of injury. If the exact cause of injury is uncertain, it is prudent to wait for about 8 weeks for signs of recovery. If this does not occur, the nerve should be explored: (a) to confirm the diagnosis and (b) to repair the lesion by direct suture or grafting. While waiting for recovery the arm is held in a sling to prevent dragging on the neck muscles. The results of early nerve repair are generally good but some patients continue to complain of shoulder fatigue during lifting and overhead activities. It may be injured in fractures of the scapula, dislocation of the shoulder, by a direct blow 11. More often it is injured during shoulder dislocation or fractures of the humeral neck. Iatrogenic injuries occur in transaxillary operations on the shoulder and with lateral deltoid-splitting incisions. It is sometimes injured at the same time as the suprascapular nerve in shoulder dislocation. Simultaneous rupture of the rotator cuff can add to the diagnostic confusion by causing weak or absent arm abduction after shoulder dislocation. Retropulsion (extension of the shoulder with the arm abducted to 90 degrees) is impossible. Treatment Nerve injury associated with fractures or dislocations recovers spontaneously in about 80 per cent of cases. Excision of the nerve ends and grafting are usually necessary; a good result can be expected if the nerve is explored within 3 months of injury. Wrist extension is preserved because the branch to the extensor carpi radialis longus arises proximal to the elbow. High lesions occur with fractures of the humerus or after prolonged tourniquet pressure. There is an obvious wrist drop, due to weakness of the radial extensors of the wrist, as well as inability to extend the metacarpophalangeal joints or elevate the thumb. Sensory loss is limited to a small patch on the dorsum around the anatomical snuffbox. In addition to weakness of the wrist and hand, the triceps is paralysed and the triceps reflex is absent. Treatment Open injuries should be explored and the nerve repaired or grafted as soon as possible. Closed injuries are usually first or second degree lesions, and function eventually returns. In patients with fractures of the humerus it is important to examine for a radial nerve injury on admission, before treatment and again after manipulation or internal fixation. If the palsy is present on admission, one can afford to wait for 12 weeks to see if it starts to recover. The results, even with delayed surgery and quite long grafts, can be gratifying as the radial nerve has a straightforward motor function. Clinical features Low lesions are usually due to fractures or dislocations at the elbow, or to a local wound. Iatrogenic lesions of the posterior interosseous nerve where it winds through the supinator muscle are sometimes seen after operations on the proximal end of the radius. While recovery is awaited, the small joints of the hand must be put through a full range of passive movements. If recovery does not occur, the disability can be largely overcome by tendon transfers: pronator teres to the short radial extensor of the wrist, flexor carpi radialis to the long finger extensors and palmaris longus to the long thumb abductor. Hypothenar and interosseous wasting may be obvious by comparison with the normal hand. Finger abduction is weak and this, together with the loss of thumb adduction, makes pinch difficult. Unexplained lesions of the distal (motor) branch of the nerve may be due to compression by a deep carpal ganglion or ulnar artery aneurysm. It is important to be aware of this condition in patients who start complaining of ulnar nerve symptoms some 11 Peripheral nerve disorders (a) (b) 11. Ask the patient to spread his fingers (abduct) as strongly as possible and then force his hands together with the little fingers apposed; the weaker side will collapse (the left hand in this case). In the right hand, because the adductor pollicis is weak, the patient grips the card only by acutely flexing the interphalangeal joint of the thumb (flexor pollicis longus is supplied by the median nerve). If there is no recovery after nerve division, hand function is significantly impaired.

In an actively growing cyst arrhythmia journal purchase 40mg innopran xl mastercard, there is osteoclastic resorption of the adjacent bone prehypertension examples buy discount innopran xl 80 mg on-line. Treatment Treatment depends on whether the cyst is There is always the risk that the cyst will recur and more than one operation may be needed heart attack mike d mixshow remix discount innopran xl 80 mg otc. Asymptomatic lesions in older children can be left alone but the patient should be cautioned to avoid injury which might cause a fracture arrhythmia ekg purchase innopran xl 80mg on-line. If the cyst goes on enlarging heart attack zippo lighter 80mg innopran xl amex, or if there is a pathological fracture blood pressure medication with little side effects buy cheap innopran xl 40mg online, the cavity should be thoroughly cleaned by curettage and then packed with bone chips, but great care should be taken not to damage the nearby physeal plate. If the risk of fracture is thought to be high, prophylactic internal fixation should be applied. Usually it arises spontaneously but it may appear after degeneration or haemorrhage in some other lesion. X-rays show a well-defined radiolucent cyst, often trabeculated and eccentrically placed. In a growing tubular bone it is always situated in the metaphysis and therefore may resemble a simple cyst or one of the other cyst-like lesions. In an adult an aneurysmal bone cyst may be mistaken for a giant-cell tumour (a) (b) (c) (d) 9. Looks cystic but it is actually a radiolucent benign tumour; always in the metaphysis; hard boundary tailing off towards the diaphysis. Hardly ever appears before epiphysis has fused, the pathognomonic feature is that it extends right up to the subarticular bone plate; sometimes malignant. Pathology hurry to re-operate; the lesion occasionally heals spontaneously (Malghem et al. When the cyst is opened it is found to contain clotted blood, and during curettage there may be considerable bleeding from the fleshy lining membrane. Histologically the lining consists of fibrous tissue with vascular spaces, deposits of haemosiderin and multinucleated giant cells. Occasionally the appearances so closely resemble those of giant-cell tumour that only the most experienced pathologists can confidently make the diagnosis. It is hardly ever seen before closure of the nearby physis and characteristically it extends right up to the subarticular bone plate. The patient is usually a young adult who complains of pain at the end of a long bone; sometimes there is slight swelling. A history of trauma is not uncommon Treatment the cyst should be carefully opened, thor- oughly curetted and then packed with bone grafts. Sometimes the graft is resorbed and the cyst recurs, necessitating a second or third operation. X-rays show a radiolucent area situated eccentrically at the end of a long bone and bounded by the subchondral bone plate. The endosteal margin may be quite obvious, but in aggressive lesions it is ill-defined. The centre sometimes has a soap-bubble appearance due to ridging of the surrounding bone. The cortex is thin and sometimes ballooned; aggressive lesions extend into the soft tissue. This can be done either as a frozen section before proceeding with operative treatment or (especially if a more extensive operation is contemplated) as a separate procedure. More aggressive tumours, and recurrent lesions, should be treated by excision followed, if necessary, by bone grafting or prosthetic replacement. Aggressive lesions have a poorly defined edge and extend well into the surrounding bone. Histologically the striking feature is an abundance of multinucleated giant cells scattered on a background of stromal cells with little or no visible intercellular tissue. Aggressive lesions tend to show more cellular atypia and mitotic figures, but histological grading is unreliable as a predictor of tumour behaviour. There is a high risk of metastasis and treatment requires wide, or even radical, resection. Eosinophilic granuloma is the commonest of these conditions, and the only one presenting as a pure bone lesion. Marrow-containing bone is resorbed and one or more lytic lesions may appear in the flat bones or the metaphyses of long bones. The patient is usually a child; there is seldom any complaint of pain and the condition is discovered incidentally or after a pathological fracture. X-ray shows a well-demarcated oval area of radiolucency within the bone; sometimes this is associated with marked reactive sclerosis. There may be multiple lesions and in the skull they have a characteristic punched-out appearance. Vertebral collapse may result in a flat wedge (vertebra plana) which is pathognomonic. Occasionally, however, a solitary lesion may herald the onset of one of the generalized disorders (see below). Operation is usually done to obtain a biopsy; if the lesion is easily accessible it may be completely excised or curetted; if not, radiotherapy is effective. The patient is a child, usually with widespread lesions involving the skull, vertebral bodies, liver and spleen. Individual lesions can be treated by curettage or radiotherapy; however, complete remission is very unlikely. They are usually symptomless and discovered accidentally when the back is x-rayed for some other reason. However, if the patient does have backache, the haemangioma is likely to be blamed. Other sites include the skull and pelvis where the appearance occasionally suggests malignancy, but there is no associated cortical or medullary destruction. If operation is needed there is a risk of profuse bleeding, and embolization may be a useful preliminary. Less common varieties are juxtacortical chondrosarcoma, clear-cell chondrosarcoma and mesenchymal chondrosarcoma. Central chondrosarcoma the tumour develops in the medullary cavity of either tubular or flat bones, most commonly at the proximal end of the femur or in the innominate bone of the pelvis. X-rays show an expanded, somewhat radiolucent area in the bone, with flecks of increased density due to calcification within the tumour. Aggressive lesions may take on a globular appearance with scalloping or destruction of the cortex. When a benign medullary chondroma (enchondroma) undergoes malignant transformation, it is difficult to be sure that the lesion was not a slowly evolving sarcoma from the outset. Usually the progression involves contiguous bones, but occasionally multiple sites are affected. Occasionally, however, the process spreads to vital structures and the outcome is fatal. The highest incidence is in the fourth and fifth decades and men are affected more often than women. These tumours are slow-growing and are usually present for many months before being discovered. Although chondrosarcoma may develop in any of the bones that normally develop in cartilage, almost 50 per cent appear in the metaphysis of one of the long tubular bones, mostly in the lower limbs. Despite the relatively frequent occurrence of benign cartilage tumours in the small bones of the hands and feet, malignant lesions are rare at these sites. Chondrosarcomas take various forms, usually designated according to: (a) their location in the bone (central or peripheral); (b) whether they develop without precedent (primary chondrosarcoma) or by malignant change in a pre-existing benign lesion (secondary chondrosarcoma); and (c) the predominant cell type in the tumour. Exostoses of the pelvis and scapula seem to be more susceptible than others to malignant change, but perhaps this is simply because the site allows a tumour to grow without being detected and removed at an early stage. Xrays show the bony exostosis, often surmounted by clouds of patchy calcification in the otherwise unseen lobulated cartilage cap. A tumour that is very large and calcification that is very fluffy and poorly outlined are suspicious features, but the clearest sign of malignant change is a demonstrable progressive enlargement of an osteochondroma after the end of normal bone growth. The dominant cell type is chondroblastic but there may also be sparse osteoid formation, leading one to doubt whether this is a cartilage tumour or a non-aggressive osteosarcoma. Clear-cell chondrosarcoma There is some doubt as to whether this rare tumour is really a chondrosarcoma. However, despite the fact that it is very slow-growing, it does eventually metastasize. Pale glistening cartilage tissue was found in the medullary cavity and, in several places, spreading beyond the cortex. It tends to occur in younger individuals and in about 50 per cent of cases the tumour lies in the soft tissues outside an adjacent bone. The x-ray appearances are similar to those of the common types of chondrosarcoma but the clinical behaviour of the tumour is usually more aggressive. There is a tendency for these tumours to recur late and the patient should therefore be followed up for 10 years or longer. It is said to occur predominantly in children and adolescents, but epidemiological studies suggest that between 1972 and 1981 the age of presentation rose significantly (Stark et al. It may affect any bone but most commonly involves the long-bone metaphyses, especially around the knee and at the proximal end of the humerus. Pain is usually the first symptom; it is constant, worse at night and gradually increases in severity. In later cases there is a palpable mass and the overlying tissues may appear swollen and inflamed. Staging If a chondrosarcoma is suspected, full staging procedures should be employed. However, low-grade chondrosarcoma may show histological features no different from those of an aggressive benign cartilaginous lesion. High-grade tumours are more cellular, and there may be obvious abnormal features of the cells, such as plumpness, hyperchromasia and mitoses. Treatment Since most chondrosarcomas are slow-growing and metastasize late, they present the ideal case for wide excision and prosthetic replacement, provided it is certain that the lesion can be completely removed without exposing the tumour and without causing an unacceptable loss of function; in that case amputation may be preferable. In some cases isolated pulmonary X-rays the x-ray appearances are variable: hazy osteolytic areas may alternate with unusually dense osteoblastic areas. Diagnosis and staging In most cases the diagnosis can be made with confidence on the x-ray appearances. Radioisotope scans may show up skip lesions, but a negative scan does not exclude them. About 10 per cent of patients have pulmonary metastases by the time they are first seen. A biopsy should always be carried out before commencing treatment; it must be carefully planned to allow for complete removal of the tract when the tumour is excised. Areas of bone loss and cavitation alternate with dense patches of abnormal new bone. There may be obvious spread into the soft tissues with ossification at the periosteal margins and streaks of new bone extending into the extraosseous mass. The histological appearances show considerable variation: some areas may have the characteristic spindle cells with a pink-staining osteoid matrix; others may contain cartilage cells or fibroblastic tissue with little or no osteoid. Several samples may have to be examined; pathologists are reluctant to commit themselves to the diagnosis unless they see evidence of osteoid formation. Treatment the appalling prognosis that formerly attended this tumour has markedly improved, partly as a result of better diagnostic and staging procedures, and possibly because the average age of the patients has increased, but mainly because of advances in chemotherapy to control metastatic spread. However, it is still important to eradicate the primary lesion completely; the mortality rate after local recurrence is far worse than following effective ablation at the first encounter. After clinical assessment and advanced imaging, the patient is admitted to a special centre for biopsy. Depending on the site of the tumour, preparations would have been made to replace that segment of bone with either a large bone graft or a custommade implant; in some cases an amputation may be more appropriate. The pathological specimen is examined to assess the response to preoperative chemotherapy. Pulmonary metastases, especially if they are small and peripherally situated, may be completely resected with a wedge of lung tissue. Outcome Long-term survival after wide resection and chemotherapy has improved from around 50 per cent in 1980 (Rosen et al. There is a fairly high complication rate (mainly wound breakdown and infection) but, in patients who survive, 10-year survival with mechanical failure as the end point is 75 per cent and for failure for any cause is 58 per cent. Treatment For a low-grade parosteal osteosarcoma, wide excision without adjuvant therapy is sufficient to ensure a recurrence rate below 10 per cent. Dedifferentiated parosteal osteosarcoma should be treated in the same way as intramedullary sarcoma. It is more like an intramedullary osteosarcoma, but situated on the surface of the bone. The appearances sometimes suggest a periosteal chondroma and the diagnosis may not be certain until a biopsy is performed. The patient is a young adult who presents with a slowly enlarging mass near the bone end. X-ray shows a dense bony mass on the surface of the bone or encircling it; the cortex is not eroded and usually a thin gap remains between cortex and tumour. The picture is easily mistaken for that of a benign bone lesion and the diagnosis is often missed until the tumour recurs after local excision. Although the lesion is outside the bone, it does not spread into the adjacent muscle compartment until fairly late. Pathology At biopsy the tumour appears as a hard Histologically this is a true osteosarcoma, but characteristically the sections show a prominent cartilaginous element.

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