The surgery of tuberculosis
From Primary Surgery
Chemotherapy for tuberculosis
In addition to treating pulmonary tuberculosis, you may have to treat 'surgical' tuberculosis in a patient's lymph nodes (30.2), his bones and joints (30.3), his abdomen (30.5), his urinogenital tract (30.6), and in a woman's breasts, where it can present as a lump (21.3), or as an oedematous swelling, due to the involvement of her axillary nodes (31.6). Diagnosing tuberculosis can be difficult. In the developing world, and particularly if BCG has been given, a positive tuberculin test strengthens the diagnosis, only if it is strongly positive (for example Mantoux test > 30 mm at 72 hours). A persistently negative one makes the diagnosis of tuberculosis unlikely, unless the patient is severely ill (as with miliary tuberculosis), is HIV-positive (see below), or is very malnourished, or has some other severe illness.
If you can send tissue for histology, especially a lymph node, the diagnosis of tuberculosis is easily confirmed. If this is impossible,or will take too long, you can usually tell if tissue is tuberculous, by cutting it across and looking for caseous areas. Finally, "If you can't think of a diagnosis, always remember the possibility of tuberculosis".
The same drugs that are used for pulmonary tuberculosis are highly successful in surgical tuberculosis—if a patient takes them regularly, and completes the course. The great danger is that he will stop taking them as soon as he feels a little better. The regime that you choose to use will have to depend on: (1) how much money there is for drugs, (2) how easy it will be for him to attend a clinic for injections of streptomycin, (3) if (based on (1) and (2)) you decide to admit him, and (4) it drug resistance is likely. It is unlikely, except in patients who have been partly treated before. We give several alternative regimes below, and there will probably be a standard one in your area. Most regimes have an initial intensive phase, followed by a continuation phase. Never treat tuberculosis with a single drug, because of the risk of acquired resistance.
Isoniazid is the main drug, and if rifampicin were not so expensive,it would be the best companion drug to go with it. Because it is so expensive, you will probably have to use thiacetazone with isoniazid in a compound tablet. Thiacetazone is widely used in Africa, but some communities elsewhere show an unacceptably high frequency of adverse reactions to it. Fortunately,the prices of rifampicin and ethambutol are falling. In India, streptomycin, IN AH, and thiacetazone are provided free at tuberculosis centres; the difficulty is getting patients to go to them. Unfortunately, there are times when even these drugs are not available.
Supervise a patient carefully. If he does not complete his course of treatment, the organisms infecting him may become resistant, his disease may progress, and he may need extensive surgery—if he can get it. If he fails to attend for outpatient treatment, see that somebody visits him at home.
Treat surgical tuberculosis with drugs, and try not to drain tuberculous abscesses, unless you have to. If they have to be drained,close the wound without inserting a drain. For a tuberculous spine, or a large joint, use a suction drain. The danger is that they may become secondarily infected. Before the introduction of chemotherapy, draining a tuberculous abscess often led to a persistent sinus, and was sometimes fatal.
HE MUST CONTINUE TO TAKE HIS DRUGS
HIV and tuberculosis. Highly pathogenic organisms, such as Mycbacterium tuberculosis may infect HIV-positive patients early, before immune deficiency has fully developed. Less virulent ones, such as Mycbacterium avium-intracellulare, strike later, when immune deficiency is complete. Tuberculosis may thus precede AIDS by several months. The risk of an HIV-positive patient acquiring tuberculosis depends on the prevalence of the disease in the local population. In Zambia, where both diseases are common, about 50% of new tuberculous patients are HIV-positive, commonly with multibacillary forms of the disease.
Fever, fatigue, and weight loss are common in both diseases. In an HIV-positive patient, tuberculosis affects the lungs less often than other parts of the body, and may become widely disseminated to involve: the lymph nodes (these cannot be distinguished from those enlarged by HIV alone), the joints, the spine, the blood (miliary tuberculosis), the genitourinary tract, the liver, the peritoneum, and the central nervous system (tuberculomas, cerebral abscesses, and meningitis). There may be little or no granuloma formation, and few lymphocytes in the lesions (reactive tuberculosis).
The X-ray appearances of pulmonary tuberculosis are often atypical in an HIV-positive patient. His hilar and mediastinal lymph nodes are commonly enlarged, as are his middle or lower lobes, while his upper ones are spared; cavitation is rare. There is only a 40% chance that he is tuberculin-positive, and when he is, the reaction is weak and often becomes negative later.
Give him a standard course of treatment. Bacilli will probably disappear from his sputum in one to three months. Treat him for 9 months, and consider giving him daily isoniazid after that to prevent relapse. HIV increases the incidence of adverse drug reactions, particularly, it is said, to thiacetazone, so suspect HIV when these occur.
IF YOU CAN'T THINK OF A DIAGNOSIS, THINK OF TUBERCULOSIS
CHEMOTHERAPY FOR TUBERCULOSIS
ISONIAZID (INH). Daily dose 300 mg, children 10 mg/kg. Intermittent adult dose 15 mg/kg, with pyridoxine 10 mg per dose to prevent neurotoxicity.
THIACETAZONE. Daily dose 150 mg, children 4 mg/kg.
STREPTOMYCIN. Daily dose: if a patient is less than 50 kg give him 750 mg daily, if he is more than 50 kg give him 1 g daily if he is under 40, and 750 mg daily if he is over 40; children 20 mg/kg. The disadvantage of streptomycin is that it has to be injected, but in some communities injections are best.
RIFAMPICIN. Daily dose: less than 50 kg give the patient 450 mg, more than 50 kg give him 600 mg; children 10 to 20 mg/kg. Intermittent adult dose 600 to 900 mg.
PYRAZINAMIDE. Daily dose, less than 50 kg give him 1.5 g, more than 50 kg give him 2.0 g; children 30 mg/kg. Intermittent dose 3 times a week: give him 2.0 g if he is less than 50 kg, and 2.5 g if he is more than 50 kg. Intermittent dose twice a week: give him 3.0 g if he is less than 50 kg, and 3.5 g if he is more than 50 kg.
ETHAMBUTOL. Daily dose 25 mg/kg for 2 months, then 15 mg/kg; children as for adults if aged 12 years or more. Intermittent dose three times a week 30 mg; twice a week 45 mg.
REGIMES
(1) Daily throughout. The common regime in India and in East and Central Africa is daily streptomycin for 60 days at 20 mg/kg. Starting at the same time, give thiacetazone and INH as a compound tablet (Thiazina' or Msozone Forte') for 12 or 18 months. For an adult this contains thiacetazone 150 mg (3 mg/kg) and INH 300 mg (6 mg/kg). It has a 92% success rate in previously untreated cases—if he completes the course. The drugs for the entire course cost $30. You may occasionally have to admit him to give him his streptomycin, which will add to the cost, but the cost of 2 months' admission is low compared with the cost of rifampicin.
(2) Daily throughout. Two months of daily streptomycin, isoniazid, rifampicin, and pyrazinamide, followed by 6 months of daily isoniazid and thiacetazone. Total duration 8 months, success rate 98%.
(3) Partly intermittent. Streptomycin, isoniazid, rifampicin, and pyrazinamide daily for 2 months. Then streptomycin, isoniazid, and pyrazinamide twice a week for 6 months. Total duration 8 months. (4) Intermittent throughout. Streptomycin, isoniazid, rifampicin, and pyrazinamide 3 times a week for 4 months, then isoniazid, rifampicin, and pyrazinamide 3 times a week for 2 months. Total duration 6 months.
CAUTION! Always aim to give antituberculous treatment as a complete regime. Shorter courses are likely to be ineffective,and promote drug-resistance.
ADMISSION. If he does not live near a clinic, where he can get injections, admit him to give him his streptomycin.
NO ADMISSION. If you are not going to admit him, and can afford rifampicin, use one of the intermittent regimes. They all contain isoniazid, rifampicin, and pyrazinamide. If giving him an injection is likely to encourage his compliance, then the regime should contain streptomycin. A completely oral intermittent regime of ethambutol, isoniazid, rifampicin, and pyrazinamide is equally effective, but more expensive.
If cost is critical, give him regime (1). But if he lives near a clinic, a fully supervised regime like regime (3) is likely to prove more successful and less toxic.
If cost is less critical, use regime (4).
If, in the local community, there is a high prevalence of strains of bacilli which are resistant to streptomycin and isoniazid, you will have to use a four-drug regime. This is only likely to be the case when there are many people who do not complete their treatment. If so, your follow-up programme needs improvement.
TOXICITY Be aware, and make your staff aware, of the the toxic reactions Of antituberculous drugs, especially those outlined below like this.
ISONIAZID(INH). (1) Peripheral neuritis, ±30%. Painful 'hot' soles of the feet, especially in patients whose livers metabolize the drug slowly. You can usually continue treatment, if you notice the condition early. Give him piridoxine 20 or 25 mg/day. If pain forces you to stop INAH, give another drug. (2) Psychoses, ±0.5%, reversible, stop INH immediately. (3)Jaundice <0.5%, reversible if you stop INH fairly soon.
THIACETAZONE. (1)Dermatosis. 30% of light-skinned persons (Caucasians and mongoloids), ±5% of Africans. Typically itchy, black, 2 to 4 cm patches with a centre that may peel. Also, diffuse darkening of the skin with itching (less common). If noticed immediately, partially reversible.
STREPTOMYCIN. (1)Rash ±5%, typically small widespread maculopapules usually accompanied by fever. Stop the drug.
(2) Drug fever, ±5%. Stop the drug. (3) Dysfunction of the vestibular branch of the 8th nerve (vertigo, giddiness). If mild, continue. If moderate to severe, stop the drug. (4) Dysfunction of the cochlear function of the 8th nerve {deafness). Stop immediately:irreversible unless the drug is immediately discontinued.
RIFAMPICIN. (1) Transient jaundice usually 2 or 3 weeks after starting treatment. Unless jaundice is progressive, continue the drug. Liver function tests nearly always show some abnormality. (2) If his urine becomes orange-red, this is not a sign of toxicity, it always happens. (3) Gastrointestinal symptoms, usually minor. (4) Drug fever (uncommon). (5) An MOI (monoamine oxidase inhibitor)-like action (uncommon), with intolerance to cheese, fish and meat extracts, and sensitivity to alcohol.
PYRAZINAMIDE. Arthralgia, hepatotoxicity, and urticaria are all unusual.
ETHAMBUTOL. (1) Visual impairment, ±1%, reversible if recognized quickly and the drug is stopped. Test the visual acuity (24.1) of all patients on this drug every 2 weeks, and make them aware that they must report any slight deterioration in acuity.
Tuberculous lymphadenitis
Widespread tuberculosis of the lymph nodes is not uncommon in many areas. It usually involves the nodes of the neck, or less often those of the axilla, iliac region, or groin, mainly in children and young adults, although no age is exempt. All four triangles of neck may contain matted masses of glands. If these are not treated, abscesses may form and discharge through the skin, to leave sinuses which may become secondarily infected. After many months, these abscesses may heal spontaneously, to cause severe fibrosis and lymphatic obstruction in the leg (31.4), arm, breast (31.4), or vulva (20.14).
TUBERCULOUS LYMPHADENITIS. Biopsy a lymph node to confirm the diagnosis. You may find that tuberculous lymphadenitis is so common that you cannot biopsy every suspect node. But remember that biopsy is simple, and needs only local anaesthesia.
Give chemotherapy (30.1). Don't excise the enlarged nodes. Don't be alarmed if they enlarge temporarily during chemotherapy, or, rarely, after it, without microbiological relapse. This is due to hypersensitivity to tuberculoprotein. All nodes become smaller in time.
Tuberculous bones and joints
When tuberculosis involves a patient's skeleton, it is the involvement of his joints that matters most—his spine, hips, knees, feet, elbows, wrists, and shoulders, in this order of frequency, and occasionally his other joints also. Bacilli reach his joints from some focus elsewhere. So look for lesions in his lungs, and for signs of surgical tuberculosis in other parts of his body. Look particularly for enlargement of his lymph nodes.
He is usually a young adult, or a child over 6 years, although children as young as a year and older people can also be infected. He complains that one or more of his joints has become progressively painful and stiff during the previous few weeks. If his leg is involved, his first complaint is a limp. His infected joint fills with fluid, and the muscles round it waste. He usually has only mild to moderate pain, except on forced movement. Tuberculous arthritis is 'cola, which means that the skin over his infected joint is the same temperature as his normal skin. His joint is not 'hot', as it is in septic arthritis. Sometimes he has systemic symptoms, such as mild fever, night sweats, or loss of weight or appetite. Pain and fever may be quite marked. He may also have signs of tuberculosis in his chest, or a family history of it.
In a synovial joint, the disease starts in the synovium and grows slowly over the cartilage; it then extends through the cartilage into the underlying bone, which decalcifies. In the spine, disease starts in a disc. If you can treat him before his cartilage is destroyed, his joint will recover fully, or nearly so. If you start later, his articular cartilage will be destroyed, so that even if his disease is arrested, his joint will develop a fibrous ankylosis (except in the spine, when ankylosis is always bony). Sometimes, cold abscesses and sinuses form, become secondarily infected, and may track for a considerable distance.
If a tuberculous joint is secondarily infected, the ankylosis that results is always bony.
His diseased limb develops a flexion contracture, and its joints may subluxate or dislocate, especially his hip, knee, shoulder, or elbow.
You can treat tuberculous joints successfully and cheaply—if you diagnose them early enough, and can make sure that a patient takes his drugs. 'Early', here means the first few weeks. But even if treatment starts late, when his joint surfaces have already been destroyed, he can expect a fairly good result—if you can prevent deformities and contractures.
There are no certain diagnostic signs, so the secret is always to be suspicious. Whenever you see any chronic bone or joint disease, ask yourself: "Might this be tuoerculous?" If it is, you can treat it. Biopsying a node or the synovium will confirm the diagnosis in about half the cases (see below). If you cannot send tissue for biopsy, you will probably have to rely on the characteristic X-ray changes. Even so, your error rate should be small.
Try to: (1) Give him the drugs he needs in adequate doses for an adequate period—much the most important. (2) Rest his joint; if his arm is involved, you can usually treat it in a sling, but if he has tuberculosis of his leg, you will probably have to admit him. (3) If he has disease of his hip or knee, apply traction. This will overcome spasm, prevent his softened bone from collapsing, and keep his inflamed joint surfaces apart. Experts can do major operations to remove or drain a tuberculous lesion, or promote ankylosis. For these, you will have to refer him.
TUBERCULOUS ARTHRITIS
X-RAYS. Look for: (1) Generalized rarefaction—the patient's whole joint is less dense than it should be. The earliest stage is a lack of definition—his joint is not as sharp as it should be. (2) Localized areas of erosion or decreased density, caused by caseous lesions in the bone. (3) The joint space may be abnormally narrow or wide. (4) In late cases it is irregular.
CAUTION! Joint destruction in tuberculosis is always more severe than the X-ray appearances suggest. (2) Remember to X-ray his lungs.
SPECIAL TESTS. (1) A positive tuberculin test is only of limited value (30.1).
(2) If a joint is swollen, aspirate it by the methods in Section 7.17, and examine the fluid as in Section 79.3. Great patience may occasionally find AAFB in a stained film of the exudate. Most laboratories reckon that this is not worth doing. If possible,send the fluid for culture, and guinea-pig inoculation (even then it is not always positive). You will not know the answer for several weeks.
(3) If he has any enlarged lymph nodes that might be tuberculous, biopsy one. The biopsy of synovial tissue is indicated in special cases only. Taking a biopsy from his spine is difficult, but you may be able to take one from his hip. Use the anterolateral approach, as for septic arthritis (7.18). Biopsy his knee by the methods in Section 7.17. When you take a biopsy, use the opportunity to examine his articular cartilage. A biopsy is useful for distinguishing tuberculosis from late, imperfectly-treated staphylococcal arthritis.
CAUTION! Biopsies are fallible, so accept a negative biopsy with caution. About 50% of cases of tuberculous synovitis are reported as 'non-specific chronic inflammation'.
DIFFERENTIAL DIAGNOSIS. Septic arthritis is the main one.
Suggesting septic arthritis —a history of onset over hours or days, rather than weeks; a 'hot' joint, which is acutely painful to move in any direction. He is Mil', with a high fever and a leucocytosis. Aspiration produces frank pus, rather than slightly cloudy fluid. Bacteria (usually staphylococci) are visible in a Gram stained film. If septic arthritis has been partly treated, diagnosing it may be difficult.
If his hip is involved, flex his knee to 90° and then flex his hip. If his leg goes into external rotation, as you do this, as in Fig. 7-17, it is a sign that his upper femoral epiphysis is slipping. This is much more likely to happen in septic arthritis (or spontaneous slipping of the epiphysis, 77.10) than it is in tuberculosis.
Both tuberculosis and septic arthritis eventually involve the bone of the pelvis. If it is already involved when you first see him, this suggests tuberculosis.
Suggesting trauma—a history of injury, or a haemarthrosis: the X-ray may be normal, or show widening of the joint.
Suggesting other forms of arthritis—a history of dysentery, brucellosis, or gonorrhoea.
If a Joint looks like tuberculosis, but tests are negative, he may have rheumatoid arthritis presenting in a single joint. Other joints may flare up later. If possible, take a biospy, do a Rose-Waaler test, and/or a latex test. Remember that tuberculosis is commoner than monarticular rheumatism in most of the developing world.
If he is a child and his hip is involved, consider Perthes' disease (27.14), or a slipped epiphysis (77.10).
If he is old, or had an injury previously, consider the possibility of osteoarthritis and look for lipping, areas of increased density (eburnation), and sometimes associated cysts (especially in his hip).
TREATMENT FOR SURGICAL TUBERCULOSIS. Start by admitting him in order to: (1) Confirm the diagnosis. (2) Give him the confidence that he can be cured. (3) Convince him that he needs long-term treatment. (4) Apply traction to his lower limb, if this is needed. (5) Give him his initial course of streptomycin, if he lives far from a clinic.
CHEMOTHERAPY. Treat him as in Section 30.1. Do all you can to persuade him to continue treatment to the end. Review him regularly. When his course of treatment is completed, warn him that his joint may flare up again at any time. If so, he must return for further treatment. POSITION OF FUNCTION. The range of movement of his joint may be limited or absent, so make sure that it is kept in the position of function in Fig. 7-16.
ANKYLOSIS. A fibrous ankylosis may be acceptable, even in his leg, especially if he is a child. It is also acceptable in his arm, provided it is near the optimum position of function-see Fig. 7-16.
PARTICULAR JOINTS INFECTED BY TUBERCULOSIS SHOULDER. Aim for a loose fibrous ankylosis. Rest his arm in a sling, and then gradually encourage him to do without it. if it is painful at the end of treatment, refer him for an arthrodesis. This will not be a significant disability, because of his scapulo-humerai movement.
ELBOW An elbow fixed in the position of function as in Fig. 7-16, is likely to be better than a stiff painful one. If non-operative treatment fails to give him a pain-free elbow, refer him for an excision/arthroplasty. This will give him a considerable range of movement, but little stability. Fusion is rarely necessary.
HIP. He is usually a child who presents with a painful hip or a limp. For the differential diagnosis, see Section 27.13. Symptoms may start slowly, but he ultimately becomes ill, and fretful,with painful restriction of the movements of his hip. To begin with it is flexed and abducted; later it is flexed and adducted, his leg is shortened, his thigh is wasted, and he may have abscesses in his buttock or groin, as in Fig. 29-1. There is loss of joint space, and a characteristically severe rarefaction of the bone round his hip. If possible, aspirate or explore it, so as to confirm the diagnosis bacteriologically.
Give him chemotherapy and rest his hip, at first in bed only, and then, when pain is a little less, apply skin traction (70.10). If there is abscess formation, and the whole of the head of his femur is necrotic (uncommon in tuberculosis), refer him for the removal of necrotic tissue.
If his hip is in spasm (as diagnosed by rolling it), or his hip or knee show any flexion deformity, apply extension traction (78.3) for several weeks. This will control pain and prevent a flexion contracture.
If there is only narrowing of the joint space, and no bony destruction, allow him up, usually after about 2 months, and let him use his leg cautiously, starting with partial weight bearing,using crutches and a patten (raised shoe) on his normal leg to keep his diseased one off the ground. Skin traction should have corrected any flexion contracture (if present) by this time.
If there is considerable bony destruction, especially of the head of his femur, he still has some hope of a reasonably functioning joint. Don't worry about whether his ankylosis is fibrous or bony. Apply skin traction for 3 months and then get him up on crutches.
Alternatively, and less satisfactorily, put him into a hip spica, in the position of function (7-16). Start him on full weight-bearing. After 3 months, remove his spica and fit him with a removable splint of plaster, leather, or metal, which he can take off for bath or bed. He may need some kind of splint permanently,or until his hip has fixed.
if, after 4 to 6 months, he still has a painful joint with very limited movement or no movement, except under anaesthesia (unusual), consider referring him for operative arthrodesis of his knee, or of his hip. Both these operations should be done during the first two years, while he is stitl on chemotherapy.
KNEE He presents with a limp, miid pain, a swollen knee, marked wasting of his quadriceps, limitation of movement (especially extension), and a flexion deformity.
Put him into a Thomas splint, or extension skin traction (78.3), for at least 3 months, and then get him up on crutches. Gradually increase the weight his leg bears, until he is walking as well as he can. If his disease is advanced, or if his pain continues, you may have to fit him with a long leg plaster cylinder; otherwise avoid one.
If a child requires an arthrodesis of his knee, try to delay this until growth has stopped.
ANKLE. Give him chemotherapy, and apply a short leg walking cast (81.5).
TENDON SHEATHS. If he develops a chronic swelling of the tendon sheaths of his hand, or the bursae round his shoulder, don't forget that tuberculosis can involve any of the synovial membranes.
DIFFICULTIES WITH A TUBERCULOUS JOINT If his symptoms are mild so that DIAGNOSIS is DIFFICULT, you can: (1) Wait 4 to 6 weeks, before committing him to long-term treatment—provided you are sure you are not missing acute untreated septic arthritis. During this time some diseases (transient synovitis and rheumatic fever) will settle, and others may reveal themselves (partly-treated septic arthritis). Tuberculosis will not advance much during this time. (2) Explore the joint, biopsy the synovial membrane, and remove a lymph node for biopsy. An ESR may also be useful.
Alternatively, and less satisfactorily, you can start a trial of treatment with streptomycin and isoniazid for a month. If your diagnosis was correct, the spasm in the muscles round his tuberculous joint will become less, and his general symptoms will improve.
If you are not sure if he has septic arthritis, or tuberculosis, even after opening the joint, treat him for both, and review him later when the histological report is available.
If DEFORMITY PREVENTS SATISFACTORY WALKING, corrective surgery is essential. If an arthrodesis is needed (more likely in the knee than the hip), it is usually best done 6 to 8 weeks after chemotherapy starts.
If an OLD TUBERCULOUS JOINT IS INJURED, observe him closely. A fibrous ankylosis is always unsafe, and can flare up at any time. If pain, etc. continue, and he has no bony injury and no ligament rupture, give him another full course of chemotherapy.
If a COLD ABSCESS develops, leave it, unless it is very big and is causing pain and discomfort. All but the big ones set-tie on chemotherapy in 12 months, if you have to aspirate a cold abscess (unusual), do so repeatedly with a wide-bore needle.If you can introduce the needle through a long oblique track, a sinus is less likely to form. If it is very large, explore it, clear out its contents, and close it to prevent the entry of secondary infection.
CAUTION! Don't leave a drain in a cold abscess, or it will become secondarily infected.
If a SINUS develops, it is the result of an abscess opening on to his skin, and is a sign of low resistance. Sinuses are rare once chemotherapy has started, although an old one may open up temporarily. Chemotherapy will usually close it. A sinus may become secondarily infected, but does not require specific treatment. A biopsy from the track is unlikely to confirm tuberculosis,because non-specific granulation tissue lines it.
If a JOINT BECOMES WARM AND TENDER, with deteriorating X-ray signs, and he has general symptoms, he is experiencing a flare-up. This is unlikely to happen if he has completed his course of treatment, and is a sign that chemotherapy has failed. Consider some other disease, such as septic arthritis, gonococcal arthritis, monarticular rheumatism, or gout. Give him a further course of treatment.
If his LEG ends up SHORT, raise his shoe.
ANY PERPLEXING JOINT IS TUBERCULOUS UNTIL PROVED OTHERWISE
Tuberculosis of the spine (and idiopathic scoliosis)
The spine is the most common and the most dangerous site for skeletal tuberculosis. It takes two forms: (1) In the first, the patient's general symptoms are mild. The infection usually starts in the anterior part of a disc, and spreads to the adjacent surface of the body of a vertebra, or to two adjacent ones. It seldom involves his neural arches. The result is that, as the bodies of his vertebrae collapse, his spine angles forwards to produce a kyphus (an increase in the normal convex curve of the spine: a scoliosis is a lateral curvature). The shape of his spinal deformity depends on how many of his vertebrae are diseased. Commonly, as his deformity gets worse, a sharp angle (the gibbus)appears. Uncommonly,the destruction is not symmetrical, so that his spine rotates. (2) In the second form his general symptoms are more severe, several of his vertebrae are involved widely in his spine (including perhaps some in his neck), and his disc spaces may not be narrowed.
His first symptom is pain in his back, and his first sign is increasing kyphosis. Later, pus from his diseased vertebrae may track along tissue planes to present as a cold abscess in unexpected places, particularly in his groin (psoas abscess). He may become paraplegic (30.4a).
In a child spinal tuberculosis is an important cause of back pain. He will probably be unwell and have lost weight, but not always so. He may resent examination, be tender over his low thoracic or upper lumbar spine, and show any of the signs seen in adults.
Give him chemotherapy as an outpatient, without applying a plaster jacket. The former practice of giving all patients with spinal tuberculosis a plaster jacket is now outmoded. You will find that his spine will heal quicker if you let his vertebrae collapse down and fuse. As it does so, his pain will go and his vertebrae will recalcify. His deformity will probably increase by about 5° to 25° during treatment. Only extensive surgery, in the most expert centres, gets better results than this. Its main advantage is that it establishes bony fusion in 2 years, instead of in 4 years.
Idiopathic kyphoscoliosis is one of the differential diagnoses of a tuberculous spine. It is a disease of unknown cause, in which a child's spine slowly develops a curve. It may start as early as 3 years, but it more often starts at 7 or 8; it progresses most rapidly between the ages of 12 and 14, and gets worse until he stops growing. If possible, refer him to a special centre, which can fit him with a Milwaukee or similar brace, and if necessary fuse his spine at the appropriate time. If you cannot refer him, reassure his parents that, although he will always be a hunchback, he will be normal in most other ways. Spinal compression is rare, but a moderate or severe lesion will affect the function of his lungs by reducing the size of his thoracic cage.
SPINAL TUBERCULOSIS EXAMINATION. Examine a patient as in Section 27.8. Examine him from the side; look and feel for: (1) a kyphus, (2) reduced movement of his lumbar spine, (3) cold abscesses in his paraspinal area, loin, and groin, (4) sinuses. Test the reflexes in his legs, and their tone, power, and sensation.
X-RAYS are critical, see Fig. 29-3. X-ray his chest also. Look for: (1) Narrowing or obliteration of a joint space, involving at least two vertebral bodies and the disc between them (this is the typical late picture). Sometimes several vertebrae disappear into the space normally occupied by one or two. So count his vertebral spines, because these may be all that is left when his vertebral bodies have been destroyed. (2) Look for forward collapse of his spine. (3) You may also see: (a) the shadow produced by a paravertebral abscess in his thoracic region (this strongly suggests tuberculosis, but it can be produced by staphylococcal and other forms of bacterial osteitis), and (b) calcification in his psoas sheath, showing that a psoas abscess is forming. Evidence of a paravertebral abscess increases the probability of tuberculosis being the cause, but is not necessary for diagnosing it. (4) Osteophytes and bridging (rare). If you do see bridging, it is more likely to be due to late staphylococcal infection.
SPECIAL TESTS. The ESR is useful and may be very high. A falling ESR is an indication of response to treatment, but is less important than an improvement in his clinical condition, as indicated by decreasing pain and tenderness.
THE DIFFERENTIAL DIAGNOSIS OF A TUBERCULOUS SPINE Suggesting pyogenic osteitis—a more rapid onset, less bone destruction, and a higher temperature. Confirming the diagnosis may have to depend on the aspiration and examination of pus from his spine, or on costotransversectomy, see Section 30.4a.
Suggesting poliomyeiitis—weak, wasted, flaccid legs. If polio involves his spine, it is almost sure to involve his legs too. Scoliosis rather than kyphosis.
Suggesting idiopathic scoliosis—the curve is smooth, with no gibbus, or muscle-wasting. Apart from the curved shape of his spine, there are no other signs; his X-rays are normal, and no vertebrae are destroyed. The disease starts in childhood.
Suggesting a congenital hemivertebra causing scoliosis (usually mild)—half of one of his vertebrae is missing. The half which remains forms the apex of the curve. On an X-ray this is almost triangular, its edges are smooth and well formed, and there are no signs of disc destruction in the vertebra above or below. This kind of scoliosis does not progress with age, and needs no treatment.
Suggesting kyphoscoliosis due to lung disease—a previous history of empyema. By making his lung collapse, an empyema may collapse his thoracic cage. Other causes of fibrosis of a lung, or pneumonectomy. His spine itself needs no treatment.
Suggesting secondary deposits—involvement of the bodies of his vertebrae without involvement of their discs. His serum alkaline phosphatase is raised. If the primary is in his prostate, his acid phosphatase will be raised also.
Suggesting a senile kyphosis—an old woman with osteoporosis of all, or most, of her spine, and normal discs, which bulge into her softened vertebrae. Her kyphus is gradual. Treatment is difficult (27.8). Suggesting Burkitt's lymphoma—the patient is a child. In the endemic areas this is the commonest cause of paraplegia in children (32.3).
TREATMENT.Give him chemotherapy, as in Section 30.1. If his back is painful at first, admit him for bed rest, but allow him up if he wishes. If he can walk, encourage him to do so.
Warn him that he must continue with his drugs, and that they will take some months to have much effect. During this time, he may find his kyphoscoliosis getting worse, before it stabilizes. If he thinks your treatment is not working, he may default, and go to a traditional practitioner. If he does default, do all you can to trace him.
DIFFICULTIES WITH A TUBERCULOUS SPINE See also Section 30.3. If his CERVICAL SPINE is involved, treat him with an orthopaedic collar, or failing this, a plaster cuirasse (64-10) and chemotherapy. His spinal canal is larger in his neck than in his thoracic region, so his spinal cord is less likely to be compressed.
If he complains of CLUMSINESS, WEAKNESS, OR INCOORDINATION,he is becoming paraplegic, so see below.
Tuberculous paraplegia, costotransversectomy
If a patient with spinal tuberculosis complains of clumsiness, weakness, or incoordination of his legs, he is becoming paraplegic. Later, the voluntary power of his legs is reduced, their muscle tone is increased, and his plantar responses become extensor. Later still, he has flexor spasms, and finally contractures.
Paraplegia is the major complication of spinal tuberculosis. In early cases it is due to an inflammatory oedema round a paraspinal abscess, and later to compression. Paraplegia may be his presenting symptom, and is usually treatable. In most cases it is motor only (unless it comes on very rapidly), because the abscess presses on the anterior columns of his cord rather than on the posterior ones. Although tuberculous osteitis affects the various regions of the spine in the following order of decreasing frequency: low thoracic, lumbar, upper thoracic, and cervical, you will see tuberculous paraplegia most commonly in the thoracic region, sometimes in the cervical region, and seldom in the lumbar region. This is because the spinal canal is wide there, and the cauda equina running through it is less easily affected than the cord.
There are two types of tuberculous paraplegia: (A) The common early type is due to inflammatory oedema which responds well to chemotherapy, and surgery, if this is necessary. (B) A less common later type, due to pressure and stretching from a bony deformity, when bony union has not occurred. It is the result of no treatment, incomplete treatment, or late treatment. Its prognosis is poor with chemotherapy alone, and even with specialized surgery (not described here), it is not good.
TUBERCULOUS PARAPLEGIA THE PROGNOSIS AND MANAGEMENT are different in the two forms of the disese in Section 30.4. The patient's bowels and bladder are sometimes involved in Stage (3) below and always in Stage (4); their improvement mirrors that of his his limb muscles. If his prognosis is good he should be operated on:
(A) If his paralysis is fairly recent (< 3 months) and his deformity is <60° (common) inflammatory oedema is the likely cause, and if the indications for surgery are followed, his prognosis is good. Even if he has >60° of deformity, he is worth managing as if oedema was the cause, but his prognosis will not be so good.
(1) if his weakness is mild (•<grade 3, see 27 2), he is almost sure to recover fully.
(2) If his weakness is severe (grade 0-3) without muscle spasms, he will probably recover.
(3) if his weakness is severe with extensor spasms, he has >50% chance of a full recovery, and if not, he will probably have a partial recovery.
(4) If weakness is severe with flexor spasms, he can expect little or no recovery, and he has little chance of walking without special aids.
(B) If his paraplegia is due to pressure or stretching from a bony deformity of his neural canal (uncommon in most areas and usually of late onset), the clinical picture is the same, except that the onset of paraplegia is late when kyphosis is marked. However, even if he has marked bony deformity with no paraspinal abscess visible on X-ray, his paraplegia may possibly still be due to inflammatory oedema, so refer him for surgery if you can. If you cannot, try chemotherapy alone: but don't operate yourself, the surgery of this kind of paraplegia is too difficult.
TREATMENT FOR TUBERCULOUS PARAPLEGIA NON-OPERATIVE TREATMENT. Admit him, and put him to bed. There is a very good chance that he will recover. If chemotherapy and bed rest don't cause neurological improvement in 6 weeks (unusual), review him. Your diagnosis is likely to be wrong, but if you are sure that he is tuberculous, consider costotransversectomy.
CHEMOTHERAPY. Give this as in Section 30.1.
NURSING CARE is the same as for traumatic paraplegia, so manage his morale, his skin, his urine, and his bowels as in Section 64.13.
COSTOTRANSVERSECTOMY
INDICATIONS. Costotransversectomy is also indicated for osteomyelitis of the spine, as described in Section 7.15. (1) Paraplegia due to osteitis (usually tuberculous), provided a paraspinal abscess (tuberculous or pyogenic) can be demonstrated on X-ray. (2) A large paraspinal abscess (tuberculous or pyogenic) when there is no paraplegia. (3) To obtain tissue for histology, when the cause of an osteitis is still in doubt, after considering the clinical condition and the X-rays. If possible, refer him, if not proceed as follows.
ANAESTHESIA. (1) General anaesthesia (A 9.1). (2) Ketamine (A 8.1). You must intubate him (A 13.2) and give him a relaxant (A 14.1), because you will have to lay him prone (A 16.12) with his chest supported on pillows, and control his ventilation. A prone patient cannot breathe spontaneously unassisted.
PREPARATION. Have 2 units of blood for him in reserve. Diathermy is useful.
Find the vertebra or vertebrae most markedly involved, by noting the site of any gibbus, and examining his X-rays. Clean his back, and cover it with a laparotomy towel with a central hole, or with 4 surrounding towels.
INCISION. Stand on his left and make a 20 cm incision centred on the affected vertebrae, curved to the left, and reaching his spinous processes at each end. Raise a flap of skin and subcutaneous tissues, and turn this medially, to expose his supraspinous ligament.
CAUTION! (1) Approach the abscess from the left, so as to avoid his azygous vein (at some levels) and his vena cava. You are unlikely to damage his aorta. (2) Later, gentle dissection near his vertebral bodies will help you to avoid damaging his pleura and entering his pleural cavity.
Use a knife to divide his left trapezius near its origin from his spinous processes, and his latissimus dorsi, as this arises from his lower six thoracic vertebrae. Open the plane between his spinous processes, and his sacrospinalis muscle, by cutting at first, and then by dissecting off the muscle from the bone with a stout periosteal elevator. If he bleeds much, pack the wound tightly with a laparotomy pad, and wait up to five minutes.
Expose the transverse processes and the related ribs of his maximally involved vertebrae, together with one vertebra above and below these. Expose the whole of each transverse process and 5 cm of rib distal to its tip.
Cut the periosteum of a rib longitudinally, and elevate it with a periosteal elevator all round. This will help to separate it from the tissue covering his underlying pleura, and protect his intercostal vessels and nerve.
Cut the rib with rib cutters (or carefully with bone cutters), 3 cm from the tip of its related transverse process. Try to avoid damaging his pleura. Then resect the medial part of the rib and the transverse process at its base Repeat this for at least one other rib.
Now look for his paraspinal abscess. Insert your index finger along the side of his vertebral bodies, and separate the tissues gently. You may need some sharp dissection with scissors— if so keep very close to the bone. This will lead you to the abscess, and not to his pleura!
Tuberculous pus is watery, with debris in it. Pus from osteomyelitis is yellow and creamy. Drain and culture what you find. Pass your finger round the anterior surface of each vertebra, up and down to ensure thorough drainage.
If you find no pus, check the X-ray, you may have chosen the wrong level. If so, remove a further transverse process and its related rib and feel again.
If you still find no abscess, take some tissue from the disc space for histology. The best place to biopsy is felt more easily than seen. Use forceps designed to biopsy the cervix, or use dissecting forceps and a No. 15 blade mounted on a long handle.
CLOSURE. Preferably use suction drainage ('Redivac', 4.10). There is no need for an intercostal drain, unless you damage his pleura. Approximate his muscles to his spine by sewing his trapezius and latissimus dorsi to his supraspinous ligament with 1/0 multifilament, or chromic catgut. Close his skin with continuous 1/0 or 2/0 monofilament. Apply a dressing. Nurse him on his back and sides, changing his position 2-houriy. He should be able to turn the upper part of his body by 48 hours, but he will still need 2-hourly assistance with turning. He may show no improvement for up to 6 weeks. If he has not improved by this time, his outlook is poor. If improvement starts by 6 weeks expect it to continue for 6 months. It will be hastened and improved by the drainage of a significant abscess.
If his paraplegia continues as before, see Section 64.13. CAUTION! Avoid an indwelling catheter. If he needs help, use intermittent sterile catheterization—see Section 64.16!
If you DAMAGE HIS PLEURA, see Section 9.2D.
Abdominal tuberculosis
Abdominal tuberculosis is now rare in the industrial world, but is common in developing countries. In India and Nepal it is responsible for about 10% ofgut obstructions. You are most likely to see it when you are expecting something else.
There are three main types, and several less common ones. In Africa the order of their frequency in adults is: (1) The type which presents as ascites. (2) The plastic type, which causes intestinal obstruction. (3) The glandular type, which involves the mesenteric nodes. In India the order of frequency of these types in adults is (2), (3), (1). In children in Africa their order of frequency is (3), (1), (2).These three types are described in detail in later sections. Less commonly, you may also see:
(4) Tuberculous strictures anywhere in a patient's gut, but usually in his caecum and distal small gut, where they are caused by the shrinkage of a tuberculous ileocaecal mass to form a fibrous constriction.
(5) Tuberculous ulcers (unusual) can occur anywhere in his gut, but are most often seen in his ileum, caecum, rectum, or sigmoid colon. In his small gut, a tuberculous ulcer can cause diarrhoea. On the rare occasions when the ulcer is in his stomach or duodenum, it can closely mimic a peptic ulcer, or a carcinoma. Caseating lymph nodes will lead you to the correct diagnosis. A tuberculous ulcer may perforate his gut, or bleed; because it usually occurs distally, he usually bleeds from his rectum.
(6) Tuberculous fistulae form occasionally. All this pathology can present in so many ways, and with so few distinguishing signs, that diagnosis is difficult. With all forms of tuberculosis he loses his appetite, he loses weight, and he feels ill, just as he does with tuberculosis elsewhere. He has vague abdominal pain and tenderness, and may vomit. Depending on the type of tuberculosis he has, he may have the symptoms of abdominal swelling (the ascitic type), obstruction (the plastic type), abdominal masses (the glandular type), or bleeding or perforation (tuberculous ulcers).
If he is not obstructed, or bleeding, you can treat him medically. But you will have to operate if his gut obstructs completely (the plastic type) or, rarely, if he bleeds (tuberculous ulcers).
The ascitic type of abdominal tuberculosis
In Africa, about 70% of patients with abdominal tuberculosis present with ascites; in India only about 10% of them do. In Zambia tuberculosis is responsible for 20% of all cases of ascites. The patient presents with a swollen abdomen containing many litres of straw-coloured fluid. A child with advanced abdominal tuberculosis typically has 'a ballooned abdomen and matchstick legs', but in many children the diagnosis is far from obvious. The fluid accumulates as the result of large numbers of miliary tubercles on his peritoneum. The only certain way to make the diagnosis is to do a minilaparotomy ('minilap'), which will also enable you to diagnose cirrhosis, periportal fibrosis (due to Schistosomiasis mansoni), carcinomatosis of the peritoneum and hepatoma (usually with cirrhosis). Experts can usually diagnose miliary tuberculosis with their naked eyes; but even they can be wrong, so take a biopsy of his parietal peritoneum and/or his liver.
ASCITIC ABDOMINAL TUBERCULOSIS SPECIAL TESTS. X-ray the patient's chest, and examine his ascitic fluid. If the cell count is over 50 pi, with at least 70% lymphocytes, he is fairly likely to have tuberculous peritonitis. Your lab will be unlikely to find AAFB in it, because they are very sparse. If the fluid has fewer lymphocytes than this, his ascites is more likely to be caused by cirrhosis, or periportal fibrosis.
Measure the protein in his peritoneal fluid. In tuberculous peritonitis it is usually 3 to 10 g/l, but it may be up to 20 g/l, or higher. Most patients with >20 g/l, or more, have carcinomatosis.
If it contains more than 4 g/l of protein, it is likely to be an exudate. If it contains less than 4 g/l, it is likely to be a transudate. Cirrhosis usually produces a transudate; so does periportal fibrosis, if it produces any fluid at all (uncommon).
Blood in the fluid suggests carcinomatosis or a hepatoma.
THE DIFFERENTIAL DIAGNOSIS of ascitic tuberculous peritonitis (for the plastic type see later):
Suggesting ascitic tuberculosis—miliary nodules on the peritoneum, each about 1 to 2 mm in size, slightly raised and whitish. The nodules of carcinomatosis, which is the main differential diagnosis, are larger—usually more than 3 mm—more vascular, and more irregular. You will soon learn to distinguish them. He is not as ill as he would be with a malignant effusion of the same size.
Suggesting ascites secondary to liver disease—his liver may be enlarged, hard, and irregular, or small and hard to feel; his spleen is usually large; there are usually <4 g/l of protein in his peritoneal fluid.
Suggesting the nephrotic syndrome—his ascites is less marked than his generalized oedema. If he has ascites, he usually also has marked ascites of his abdominal wall. There are usually <4 g/l of protein in his peritoneal fluid.
Suggesting nutritional oedema (hypoproteinaemia)—other signs of protein deficiency, but these may also be present in tuberculosis. There are usually <4 g/l of protein in his peritoneal fluid.
Suggesting heart failure leading to cirrhosis and ascites—a raised jugular venous pressure, and other signs of heart failure; <4 g/l of protein in his peritoneal fluid.
Suggesting carcinomatosis of the peritoneum—hard deposits in the pouch of Douglas or rectovesical pouch; usually >20 g/l of protein in his peritoneal fluid.
A MINILAP TO DIAGNOSE THE CAUSE OF ASCITES INDICATIONS. Ascites of uncertain cause. In the developing world, especially, a patient can have more than one diagnosis, for example, cirrhosis and tuberculosis peritonitis. Ascites predominating over other signs usually requires a minilap. It is seldom indicated when the ascites is not predominant, as in the generalized oedema of heart failure, or renal disease. Check his blood urea before you proceed.
CAUTION!(1) A minilap is NOT suitable for exploring the abdomen. (2) You can diagnose tuberculous abdominal glands this way, but they are better biopsied elsewhere, for example in his axilla.
DRAINING THE ASCITES. If he has more than a mild ascites, draw off most of the ascitic fluid slowly before you begin. If it all escapes suddenly, as you open his abdomen, his circulation may collapse. So draw off one litre every 2 hours, starting 48 hours preoperatively, to a maximum of 6 litres. If there is still significant ascites, after you have withdrawn 6 litres, wait until next day before you draw off more. Use a wide-bore intravenous cannula, a drip set, and a sterile bottle.
CAUTION! To avoid possible injury to a large spleen, which may be difficult to feel because of the ascites, drain the fluid from his right lower abdomen.
ANAESTHESIA. Use local anaesthesia in an adult or ketamine in a child. Avoid general anaesthesia, because he may have cirrhosis.
INCISION. Make a 5 to 6 cm right upper muscle-splitting paramedian incision 4 or 5 cm from the midline. This will allow you to see and examine his liver, and will be less likely than a midline incision to leak ascitic fluid postoperatively.
Look for miliary tubercles and secondary deposits on his peritoneum. Tubercles are remarkably uniform in size, and fairly uniform in appearance (like salt grains). Take a biopsy from his parietal peritoneum. Take a needle biopsy of his liver under direct vision, if this is indicated (32.26), or take a wedge biopsy.Close the incision in the usual way, but don't insert a drain, or it will leak continuously.
TO BIOPSY HIS PERITONEUM remove an elliptical piece of his parietal peritoneum 2x0.5 cm, from the edge of the abdominal incision. This is only necessary if it is abnormal macroscopically.
WEDGE BIOPSY OF THE LIVER
INDICATIONS. The histological examination of any suspicious lesion in the liver.
METHOD. Insert 2 '0' chromic catgut atraumatic sutures near the anteroinferior border of his liver, as in Fig. 29-7. Tie these so as to 'squeeze' his liver, adjacent to the segment you are going to incise, to stop it bleeding. Remove a wedge of his liver 0.5 x 1.5 cm. Bring the cut edges of his liver together with two more mattress sutures, placed transverse to, and outside, the first two.
TREATMENT FOR ASCITIC TUBERCULOSIS Give him chemotherapy. Don't expect miracles, if he has acute disease and ascites. Before 2 months, the failure of the fluid to reaccumulate will show that he is improving.
The plastic peritonitis type of abdominal tuberculosis
This is the result of a tuberculous granuloma, which causes a patient's omentum, and the other structures in his abdomen, particularly loops of his distal small gut, his caecum, and his ascending colon, to mat together with many adhesions. The affected coils of his gut are thick and rubbery, with characteristic transverse lesions on his small gut. Loops of his small gut may obstruct, and be difficult to separate. Carcinoma, amoeboma, and Crohn's disease can all cause a plastic peritonitis; but in the developing world tuberculosis is more common than all these others combined. Amoebiasis makes loops of small gut stick to the descending colon, without causing a true plastic peritonitis.
The obstruction in his gut is commonly incomplete, so that his symptoms are subacute or chronic, and may have lasted months or years. The adhesions which mat the loops of his gut together are extensive and difficult to separate, so manage him non-operatively if you can. Give him chemotherapy, a light diet, or fluids only, if necessary intravenously, for a few days. A tuberculous granuloma of the small gut usually resolves without a stricture; but in the ileocaecal area fibrosis and stenosis often follow.
Occasionally, you may have to operate for persisting complete obstruction. Even then, if you know tuberculosis is the cause, you will be wise to try non-operative treatment for a few days first—if there is no strangulation. When you do operate, you may find that there is no stricture in the wall of his gut, and that you can relieve the obstruction by dividing adhesions only. This is much preferable, if it is possible, because, if you open his gut, there is always a danger that a fistula may follow. If you have to open his gut, you have a choice between: (1) A 'strictureplasty',if there is a narrow stricture in his his small gut, as in A, Fig. 29-8. (2) A local small-gut bypass (D, 29-8). (3) A bypass (ileotransversostomy) between his ileum and his transverse colon (9.6). This will relieve his obstruction, and you can refer him for definitive surgery later. (4) A right hemicolectomy (66-20). If you are skilled enough to do it, this will remove the focus of infection, and is better than an ileotransversostomy.
Avoid these common mistakes: (1) Don't try to make a diagnosis without understanding the nature of the disease. Make it by weighing up the signs and symptoms carefully. (2) Don't be too eager to start a therapeutic trial without confirming the diagnosis: he may have some other disease. He will almost certainly be well enough for a 'minilap' under local anaesthesia (29-6).
(3) If you cannot make a diagnosis, don't wait too long before exploring his abdomen. (4) If he has subacute obstruction, which does not respond to non-operative treatment, you will have to relieve it surgically. (5) If he is desperately ill, don't make meddlesome and dangerous attempts to resect grossly scarred gut, or to free difficult adhesions.
PLASTIC ABDOMINAL TUBERCULOSIS SYMPTOMS. The pattern of signs and sypmtoms described here applies to abdominal tuberculosis as it presents in India and Nepal, where the plastic type of the disease predominates. The different presentation of the ascitic type is described elsewhere (30.6).
Weight loss (all cases), the patient may have lost much weight.
Weakness, maiaise, fatigue, and anorexia (75%) are common. He may also have nausea and vomiting, fever and night sweats (60%).
Abdominal pain (90%) is usually constant, central, and not severe. If it is in his right lower quadrant, it suggests ileocaecal tuberculosis. In the ascitic type pain is often mild, and may be absent.
Symptoms of obstruction (30%) include alternating constipation and diarrhoea, cramps, and gurglings. Typically, he describes a 'ball of wind' moving in his abdomen.
Rectal bleeding is rare, but may be severe.
Steatorrhoea with pale, bulky, and offensive stools is sometimes seen.
A chronic cough and blood-stained sputum are rarer than you might expect.
SIGNS OF ABDOMINAL TUBERCULOSIS Abdominal tenderness (60%) is ill-defined, and is usually maximal in the middle of his abdomen. It is absent in about half the cases. Experts say that they can recognize a peculiar 'doughy' feeling in a tuberculous abdomen.
An abdominal mass (40%) may be present. He may have one or two well-defined tender rubbery masses, either in his ileocaecal region, or at the base of his mesentery. A mass is unusual in the ascitic type.
Signs of obstruction to his lower small gut may be acute or subacute. He is usually moderately anaemic, and he may have dependent oedema as the result of hypoproteinaemia.
X-RAYS. If you suspect acute or subacute bowel obstruction, take films in the erect and supine positions (10-6,10-7). Avoid a barium follow through in the acute stage: it may make an incomplete obstruction complete.
SPECIAL TESTS. Measure his haemoglobin and his ESR, and examine his stools. X-ray his chest, and examine his sputum. Do a tuberculin test (30.1). If he has palpable ascites, examine it as described earlier.
Examine him carefully for enlarged axillary or cervical lymph nodes; if you find one, biopsy it. An inguinal node is less likely to be diagnostic, unless it is very large.
THE DIFFERENTIAL DIAGNOSIS OF PLASTIC ABDOMINAL TUBERCULOSIS Suggesting ascaris infection—he is a child with vague abdominal pain, and subacute obstruction but no weight loss or fever. Tenderness is not constant, and palpable masses of worms are unusual. See Section 10.6.
Suggesting an appendix abscess—a short history, and an acute onset.
Suggesting amoebiasis—a history of passing blood and mucus rectally, and trophozoites in his stools.
Suggesting carcinoma of the colon—a Western life style. It does occur in villagers but is unusual.
Suggesting cirrhosis or a liver tumour—an iregularfirm or hard liver, prominent ascites, and a large spleen, a previous attack of hepatitis, alcoholism. A bruit is often present (32.26).
Suggesting Crohn's disease(rare)—loss of weight and diarrhoea are the main symptoms. The differential diagnosis may be impossible until tissues are examined histologically.
NON-OPERATIVE TREATMENT FOR ABDOMINAL TUBERCULOSIS INDICATIONS. (1) You are reasonably certain of the diagnosis. He is either not obstructed, or his obstruction is subacute. (2) There are no signs of strangulation.
REGIME. Give him chemotherapy (30.1). If he is an adult, his abdominal symptoms and masses are unlikely to respond for about 2 months, although a child may respond sooner. Don't expect chemotherapy to work miracles, if he has acute disease and ascites. If he fails to respond to tuberculosis treatment, consider the possibility of: (1) AIDS in addition to tuberculosis. (2) Carcinoma, or an abdominal lymphoma.
If he is subacutely obstructed, pass a nasogastric tube, give him intravenous fluids, and resuscitate him as in Section 10.5. If he improves and his obstruction passes off, good. If it does not, you may have to operate to divide adhesions, but there is no guarantee that they will not form again.
A DIAGNOSTIC LAPAROTOMY FOR PLASTIC ABDOMINAL TUBERCULOSIS A minilap for ascitic tuberculosis is described above. A standard laparotomy through an ordinary incision is a more extensive procedure, which may involve you in further surgery. Do one if he has a persistent vague abdominal pain, perhaps some intestinal symptoms, weight loss, and a raised ESR. Open his peritoneal cavity through a right paramedian incision, mostly below his umbilicus, and look for the findings listed above.
If you cannot find peritoneal tubercles or rubbery lymph nodes easily, take a biopsy from his parietal peritoneum. Incise his peritoneum and biopsy a lymph node. If the site of the biopsy bleeds, control it with packs or with a 3/0 figure of eight suture which underlies the bleeding point on both sides.
If you find a firm mass at his ileocaecal junction, perhaps with adhesions to adjacent structures and a normal peritoneum, the diagnosis is more difficult. Cut across an enlarged node. If you see caseous areas, you have confirmed the diagnosis. Even so, take a specimen for histology. Avoid taking a biopsy from the wall of his gut—this may lead to a fistula.
If the nature of an ileocaecal mass is uncertain, and it might be neoplastic, biopsy an enlarged node nearby and proceed as immediately below. Start chemotherapy postoperatively, and await the histological report.
If his ileocaecal mass is probably tuberculous, leave it if it is not is causing obstruction. If it is causing obstruction, do an ileotransversostomy, or if you are experienced, do a right hemicolectomy. If he is debilitated, an ileotransversostomy would be wiser, however skilled you are. Some surgeons would do one or the other of these operations whether or not the mass is causing obstruction.
If he is bleeding rectally, or has a tuberculous ulcer, treat him non-operatively if you can. Only do a hemicolectomy if bleeding is severe and continuous.
If you find a thick fibrotic segment of small gut and his ileocaecal region is normal, you can resect it and anastomose the ends if it is not too long, and there is not too much scarring or too many thick adhesions. If it is very short, do a strictureplasty as in A, Fig. 29-8.
If a tuberculous ulcer has perforated his terminal ileum, oversew and patch it, as you would with a typhoid perforation (31.8). Or, treat it by resection and end to end anastomosis (9-9).
If loops of his gut are stuck down by plastic peritonitis, don't do too much dissection—the risks are too high. Instead, if he really is obstructed, do a simple side to side entero-enterostomy. Use the same technique as an ileotransversostomy. This will bypass the diseased segment, and avoid much stressful surgery.
ILEOTRANSVERSOSTOMY FOR OBSTRUCTION DUE TO PLASTIC TUBERCULOSIS See also Section 9.3. Do it side to side, as in Fig. 9-12, but without dividing the gut and closing the ends, because there is no gut to be resected.
PREPARATION. If he is obstructed, make sure you correct his electrolytes first, as in Section 10.5. If you have time, prepare his gut. Give him a fluid diet, cleansing enemas for two days before, and a suitable course of a bowel-sterilizing agent, such as neomycin with sulphaphthalazole.
INCISION. Make a right paramedian muscle-splitting incision. Choose a point on his ileum which is at least 3 cm proximal to any stenosed or diseased gut, and apply a Babcock clamp to the antemesenteric border, lifting the gut out of the wound as you do so. Apply a second Babcock clamp about 3 cm proximal to the first one.
Reach up and draw his transverse colon into the wound. If necessary, extend the incision upwards.
Lift up the omentum which hangs below his transverse colon. It is attached to the anterior surface of his colon by a relatively bloodless fold. Divide this fold with scissors. Displace the freed omentum upwards, and so expose 6 cm of the anterior surface of his transverse colon. Place two Babcock clamps on the taenia of his colon 4 cm apart. Bring the clamps on his ileum up towards those on his colon, so the two parts of his gut lie side by side.
To minimize spillage and contamination, milk the central segment of his transverse colon empty. Then apply non-crushing clamps to each end of the denuded area. Squeeze away the contents of his ileum, and apply light occluding clamps to it in the same way.
Make a two-layer side to side anastomosis with a 3 cm stoma as in Fig. 9-12, but without resecting gut and closing the ends. Make it 2 mm from the edge of the taenia to give extra strength. Use interrupted or continuous Lembert sutures. Open his colon over a distance of about 3 cm.
Draw his omentum down and tack it lightly to the site of the anastomosis with a few interrupted sutures through the serosa only. Replace his gut in his abdomen.
The glandular type of abdominal tuberculosis
This presents as irregular lumps in a child's abdomen, sometimes with ascites, and with little tendency to obstruct. His mesenteric nodes are large, and not very mobile. They may be so large that you can feel them through his abdominal wall. They are matted together, and firm to hard, with characteristic pale yellow areas of caseation on their cut surfaces.
Often you can be fairly certain of the diagnosis. If many lymph nodes are involved, biopsy one from his neck, axilla, or groin. Non-specific adenitis is common in the groin, so only biopsy an unusually large one. You may see enlarged nodes in a chest X-ray. If you cannot establish the diagnosis in any other way, you may have to do a laparotomy and take a node for section. Lymphoma is the important differential diagnosis (32.3 and 32.4).
Urogenital tuberculosis
Suspect that a patient has tuberculosis of his urinary tract, if he has a persistent cystitis, which fails to respond to antibiotics, and has pus cells and red cells in his urine, but no bacteria are cultured from it by routine methods. He is usually a young adult without signs of tuberculosis elsewhere. Urinogenital tuberculosis is common in Asia, but is very uncommon in sub-Saharan Africa. Treatment is usually easy, cheap, and effective—if the disease is not too far advanced, and he takes his drugs conscientiously. He may improve dramatically, especially if you treat him early, and even strictures of the ureter have been known to heal. So watch for urogenital tuberculosis, and be prepared to treat him on the suspicion that he might have it. The surgery that he may need if he presents late is beyond you. Unfortunately, his disease starts so insidiously that he may not complain of it until late.
Bacilli reach one of his kidneys (usually only one, but sometimes both) in his blood, after which caseation slowly destroys it. Only when the disease has eroded into its calyces do bacilli spread in his urine down to his ureter and bladder, infect them, and cause frequency and pyuria. Eventually, most of his kidney is destroyed, after which the disease may spread outside it, to form a palpable mass in his loin, perhaps with a discharging sinus.
Tuberculosis inflames the mucosa of the bladder and forms tubercles which may ulcerate, coalesce, and form shallow ulcers, especially round the orifices of the ureters and on the trigone. Ultimately, much of the wall of the bladder is destroyed, so that it ends up scarred, red, and contracted. A ureter which drains a tuberculosis kidney is flooded with bacilli, and becomes thick, fibrosed and strictured, usually in its lower third. Above this, his urinary tract dilates to form a hydro- or pyonephrosis.
He may present with: (1) The symptoms of chronic cystitis— frequency and dysuria. Tnis later progresses to the burning nocturia and strangury of a small shrunken bladder, which may become secondarily infected. These symptoms make his bladder appear to be the cause of his disease, rather than his kidney. (2) A painless intermittent microscopic haematuria, or sometimes obvious bleeding (a renal carcinoma usually causes obvious bleeding). (3) A dull discomfort in his loin, which gets steadily worse, especially when tuberculosis is complicated by a pyogenic infection (20% of cases). His kidneys are not enlarged or tender, until late. (4) Malaise and the usual general symptoms of tuberculosis.(5) A painless, non-tender, craggy, and occasionally fluctuant tuberculous mass on one side of his scrotum. Otherwise, any genital tuberculosis he may have usually causes no symptoms.
RENAL TUBERCULOSIS EXAMINATION: Examine the patient's kidneys. Several parts of his urinary tract may be involved at the same time, so also feel his testes, his cords, and his prostate for painless non-tender enlargement. A tuberculous prostate feels irregular and D°9gy; tuberculous vesicles thick and boggy. A tuberculous epididymis feels thick, woody, and craggy, it may caseate, and form sinuses, or it may involve his testis, and cause a secondary hydrocele. His distal spermatic cord is thick and oedematous.
SPECIAL TESTS. Urine with pus cells and red cells, but no bacteria on standard culture (unless there is secondary infection),is strongly suggestive.
A 24-hour urine, or an early morning urine specimen (after a period of dehydration), may show AAFB in a stained film. Repeat the examination 3 times. This needs little equipment, but it does require considerable skill, and much time. So you will probably have to rely on finding pus cells and red cells only. If possible, culture his urine for AAFB.
If you are in an endemic area and routine examination shows no ova of Schistosoma haematobium, examine the deposit from a specimen passed at midday (the time when most ova are passed)on 3 consecutive days. He is usually anaemic, and his sedimentation rate is raised.
CYSTOSCOPY (23.3), will confirm the diagnosis, show the degree of involvement of his bladder, and exclude schistosomiasis.
X-RAYS. Look for the outline of an enlarged kidney, calcification, and obliteration of his psoas shadow.
An IVU will only be positive if disease is advanced. Look for 'moth-eaten calyces', and dilatation of his renal pelvis, and ureter. If it is very advanced, his kidney will not be functioning.
DIFFERENTIAL DIAGNOSIS, In endemic areas schistosomiasis haematobium is the main one, and is much the most common cause of pain on micturition with pus cells and red cells in the urine, compared with urinary tuberculosis, which is uncommon or rare.
Suggesting schistosomiasis—(1) small 3 to 5 mm nodules in his epididymis, nearly always in the tail. (2) Calcification of his bladder wall, as shown by a line in the shape of his bladder,which collapses after micturition. (3) Do a cystoscopy before an IVU, which is much more expensive. (4) The special test above.
TREATMENT CF RENAL TUBERCULOSIS Treat him as an outpatient, with the standard tuberculosis chemotherapy (30.1). If his renal function is impaired, avoid streptomycin, or ethambutol, or give them intermittently. Rifampicin, INH, and pyrazinamide are safe. Ask him to return every 2 months for regular assessment, including the examination of his urine, and a further supply of drugs.
If he relapses, and you think that he has not taken his drugs faithfully, consider changing to a regime using second-line drugs.
INDICATIONS FOR SURGERY Operations for renal tuberculosis are beyond the scope of this manual. Refer him.
If his IVU shows no function, or has a moth-eaten appearance, with flecks of calcium, refer him for nephrectomy. Hypertension is an additional reason. If he is toxic and febrile, suggesting that he has a pyonephrosis, or a perinephric abscess, this is urgent. Otherwise, give him 6 weeks of chemotherapy first, to improve his condition for surgery.
If he has a ureteric stricture, refer him for urological investigation before starting chemotherapy. If you cannot refer him, all you can do is to give him chemotherapy. In endemic areas, schistosomiasis is a commoner cause of a stricture.
If he still has extreme frequency and dysuria, after 3 to 6 months of chemotherapy, suspect that he has a small contracted bladder. Confirm this by cystoscopy and a cystogram. Surgery may be possible.
