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Treatments
Hair complaints
ALOPECIA
The two major forms of alopecia are
1. scarring and
2. nonscarring.
Scarring alopecia is associated with
1. fibrosis,
2. inflammation, and
3. loss of hair follicles.
A smooth scalp with a decreased number of follicular openings is usually observed clinically, but in some patients, the changes are seen only in biopsy specimens from affected areas.
In nonscarring alopecia, the hair shafts are absent or miniaturized, but the hair follicles are preserved, explaining the reversible nature of nonscarring alopecia.
In women with androgenetic alopecia, an elevation in circulating levels of androgens may be seen as a result of ovarian or adrenal gland dysfunction or neoplasm. When there are signs of virilization, such as a deepened voice and enlarged clitoris, the possibility of an ovarian or adrenal gland tumor should be considered.
Exposure to various drugs can also cause diffuse hair loss, usually by inducing a telogen effluvium. An exception is the anagen effluvium observed with antimitotic agents such as daunorubicin.
Alopecia is a side effect of the following drugs: warfarin, heparin, propylthiouracil, carbimazole, isotretinoin, acitretin, lithium, beta blockers, interferons, colchicine, and amphetamines.
Less commonly, nonscarring alopecia is associated with lupus erythematosus and secondary syphilis.
In systemic lupus there are two forms of alopecia
1. scarring secondary to discoid lesions
2. nonscarring.
The latter form coincides with flares of systemic disease and may involve the entire scalp or just the frontal scalp, with the appearance of multiple short hairs (“lupus hairs”) as a sign of initial regrowth. Scattered, poorly circumscribed patches of alopecia with a “moth-eaten” appearance are a manifestation of the secondary stage of syphilis. Diffuse thinning of the hair is also associated with hypothyroidism and hyperthyroidism.
Scarring alopecia is more frequently the result of a primary cutaneous
disorder such as lichen planus, folliculitis decalvans, chronic cutaneous (discoid) lupus, or linear scleroderma (morphea) than it is a sign of systemic disease. Although the scarring lesions of discoid lupus can be seen in patients with systemic lupus, in the majority of patients, the disease process is limited to the skin. Less common causes of scarring alopecia include sarcoidosis (see “Papulonodular Skin Lesions,” below) and cutaneous metastases.
In the early phases of discoid lupus, lichen planus, and folliculitis
decalvans, there are circumscribed areas of alopecia. Fibrosis and
subsequent loss of hair follicles are observed primarily in the center
of these alopecic patches, whereas the inflammatory process is most
prominent at the periphery. The areas of active inflammation in discoid lupus are erythematous with scale, whereas the areas of previous inflammation are often hypopigmented with a rim of hyperpigmentation.
Different Non-scarring Alopecia
1. Telogen effluvium
Diffuse shedding of normal hairs. Follows major stress (high fever, severe infection) or change in hormone levels (postpartum). Reversible without treatment. Stress causes more of the asynchronous growth cycles of individual hairs to become synchronous; therefore, larger numbers of growing (anagen) hairs simultaneously enter the dying (telogen) phase. Observation; discontinue any drugs that have alopecia as a side effect; must exclude underlying metabolic causes, e.g., hypothyroidism, hyperthyroidism.
2. Androgenetic alopecia (male pattern; female pattern)
Miniaturization of hairs along the midline of the scalp. Recession of the anterior scalp line in men and some women. Increased sensitivity of affected hairs to the effects of androgens. Increased levels of circulating androgens (ovarian or adrenal source in women)
3. Alopecia areata
Well-circumscribed, circular areas of hair loss, 2–5 cm in diameter. In extensive cases, coalescence of lesions and/or involvement of other hair-bearing surfaces of the body. Pitting or sandpapered appearance of the nails. The germinative zones of the hair follicles are surrounded by T lymphocytes. Occasional associated diseases: hyperthyroidism, hypothyroidism, vitiligo, Down syndrome
4. Tinea capitis
Varies from scaling with minimal hair loss to discrete patches with “black dots” (broken infected hairs) to boggy plaque with pustules (kerion). Invasion of hairs by dermatophytes, most commonly Trichophyton tonsurans.
5. Traumatic alopecia
Broken hairs, often of varying lengths. Irregular outline. Traction with curlers, rubber bands, braiding. Exposure to heat or chemicals (e.g., hair straighteners) Mechanical pulling (trichotillomania). Discontinuation of offending hair style or chemical treatments; diagnosis of trichotillomania may require observation of shaved hairs (for growth) or biopsy, possibly followed by psychotherapy.
Female complaints
PCOS
Polycystic ovarian syndrome (PCOS) is a syndrome manifested by amenorrhea, hirsutism and obesity associated with enlarged polycystic ovaries. This heterogeneous disorder is characterized by excessive androgen production by the ovaries mainly.
Diagnosis is based upon the presence of any two of the following three criteria (ASRM/ESHRE, 2003).
• Oligo and/or anovulation.
• Hyperandrogenism (clinical and/or biochemical).
• Polycystic ovaries.
Other etiologies (CAH, thyroid dysfunction, hyperprolactinemia, Cushing syndrome) are to be excluded.
The patient complains of increasing obesity (abdominal – 50%), Menstrual abnormalities (70%) in the form of oligomenorrhea, amenorrhea or DUB and infertility. Presence of hirsutism and acne are the important features (70%). Virilism is rare. Acanthosis nigricans is characterized by specific skin changes due to insulin resistance. The skin is thickened and pigmented (grey brown). Commonly affected sites are nape of the neck, inner thighs, groin and axilla. HAIR-AN syndrome in patients with PCOS is characterized by:
1. Hyperandrogenism,
2. insulin resistance
3. Acanthosis nigricans.
Internal examination reveals bilateral enlarged cystic ovaries which may not be revealed due to obesity. Sonography — Transvaginal sonography (TVS) is specially useful in obese patient.
LH level is elevated and/or the ratio LH: FSH is > 2:1. Raised level of estradiol and estrone. SHBG level is reduced. Raised serum testosterone (> 150 ng/dl) and DHEA–S may be marginally elevated.
Raised fasting insulin levels > 25 μIU/ml and fasting glucose/insulin ratio < 4.5 suggests IR (50%). Levels of serum insulin response > 300 μIU/ml at 2 hours postglucose (75 gm) load, suggests severe IR. Features suggestive of insulin resistance are: BMI > 25 kg/m2, Acanthosis nigricans and Waist to hip ratio > 0.85.
In about 20% cases, there may be mild elevation of prolactin level due to increased pulsitivity of GnRH or due to dopamine deficiency or both. The prolactin further stimulates adrenal androgen production.
Obesity is also associated with reduced SHBG. It also induces insulin resistance and hyperinsulinemia which in turn increases the gonadal androgen production.
Risk of hypertension and cardiovascular disease as dyslipidemia (↓HDL,↑triglycerides, ↑LDL) is the most common metabolic abnormality in women with PCOS. Obsructive sleep apnea.
FIBROID
Fibroid is the commonest benign solid tumor in female. It has been estimated that at least 20 percent of women at the age of 30 have got fibroid in their wombs. Fortunately, most of them (50%) remain asymptomatic. The incidence of symptomatic fibroid in hospital outpatient is about 3 percent. These are more common in nulliparous or in those having one child infertility. The prevalence is highest between 35–45 years.
The aetiology still remains unclear. The prevailing hypothesis is that, it arises from the neoplastic single smooth muscle cell of the myometrium, chromosomal abnormality, Role of polypeptide growth factors—Epidermal growth factor (EGF), insulin-like growth factor-1 (IGF-1), transforming growth factor (TGF), stimulate the growth of leiomyoma either directly or via oestrogen. A positive family history is often present.
It is predominantly an estrogen-dependent tumor. Estrogen and progesterone is incriminated as the cause. Estrogen dependency is evidenced by growth potentiality is limited during childbearing
Period, increased growth during pregnancy, they do not occur before menarche, following menopause, there is cessation of growth
and there is no new growth at all, It seems to contain more estrogen receptors than the adjacent myometrium, Frequent association of anovulation.
The growth potentiality is not squarely distributed amongst the fibroids which are usually multiple, some grow faster than the others. On the whole, the rate of growth is slow and it takes about 3–5 years for the fibroid to grow sufficiently to be felt per abdomen.
However, the fibroid grows rapidly during pregnancy or amongst pill users (high dose pills). Rapid growth may also be due to degeneration or due to malignant change. The newer low dose oral contraceptives are not associated with increase in the growth of a fibroid. The fibroids are mostly located in the body of the uterus and are usually multiple.
Menorrhagia (30%) is the classic symptom of symptomatic fibroid.
The menstrual loss is progressively increased with successive cycles. Increased surface area of the endometrium (Normal is about 15 sq cm). Interference with normal uterine contractility due to interposition of fibroid. Congestion and dilatation of the subjacent endometrial venous plexuses caused by the obstruction of the tumor.
Symptoms of Fibroid Uterus
Asymptomatic—majority (75%)
Menstrual abnormality: Menorrhagia, metrorrhagia
Dysmenorrhea
Dyspareunia
Infertility
Pressure symptoms
Recurrent pregnancy loss (miscarriage, preterm labor)
Lower abdominal or pelvic pain
Abdominal enlargement
Pregnancy-related problems like abortion, preterm labor and intrauterine growth restriction are high. The reasons are defective implantation of the placenta, poorly developed endometrium, reduced space for the growing fetus and placenta.
The fibroids are usually painless. Pain may be due to tumor Degeneration, torsion subserous pedunculated fibroid, extrusion of polyp or due to associated pelvic pathology.
The patient may have a sense of heaviness in lower abdomen. She may feel a lump in the lower abdomen even without any other symptom.
Pressure symptoms are rare in body fibroids. The fibroids in the posterior wall may be impacted in the pelvis producing constipation, dysuria or even retention of urine.
General examination reveals varying degrees of pallor depending upon the magnitude and duration of menstrual loss.
The fibroid of varying sizes may be confused with: (1) Pregnancy (2) Full bladder (3) Adenomyosis (4) Myohyperplasia (5) Ovarian tumor (6) TO mass.
Thyroid disorders
HYPOTHYROIDISM
Iodine deficiency remains a common cause of hypothyroidism worldwide. In areas of iodine sufficiency, autoimmune disease and iatrogenic causes are most common.
Signs and Symptoms of Hypothyroidism (Descending Order of Frequency)
SYMPTOMS
• Tiredness, weakness
• Dry skin
• Feeling cold
• Hair loss
• Difficulty concentrating and poor memory
• Constipation
• Weight gain with poor appetite
• Dyspnea
• Hoarse voice
• Menorrhagia (later oligomenorrhea or amenorrhea)
• Paresthesia
• Impaired hearing
SIGNS
• Dry coarse skin; cool peripheral extremities
• Puffy face, hands, and feet (myxedema)
• Diffuse alopecia
• Bradycardia
• Peripheral edema
• Delayed tendon reflex relaxation
• Carpal tunnel syndrome
• Serous cavity effusions
Prevalence Hypothyroidism occurs in about 1 in 4000 newborns.
It may be transient, especially if the mother has TSH-R blocking antibodies or has received antithyroid drugs, but permanent hypothyroidism occurs in the majority. Neonatal hypothyroidism is due to thyroid gland dysgenesis in 80–85%, to inborn errors of thyroid hormone synthesis in 10–15%, and is TSH-R antibody-mediated in 5% of affected newborns. The developmental abnormalities are twice as common in girls.
The majority of infants appear normal at birth, and <10% are diagnosed based on clinical features, which include prolonged jaundice, feeding problems, hypotonia, enlarged tongue, delayed bone maturation, and umbilical hernia. Importantly, permanent neurologic damage results if treatment is delayed. Other congenital malformations, especially cardiac, are four times more common in congenital hypothyroidism.
The autoimmune process gradually reduces thyroid function, there is a phase of compensation when normal thyroid hormone levels are maintained by a rise in TSH. Although some patients may have minor symptoms, this state is called subclinical hypothyroidism. Later, unbound T4 levels fall and TSH levels rise further; symptoms become more readily apparent at this stage (usually TSH >10 mIU/L), which is referred to as clinical hypothyroidism or overt hypothyroidism.
The mean annual incidence rate of autoimmune hypothyroidism is up to 4 per 1000 women and 1 per 1000 men. It is more common in certain populations, such as the Japanese, probably because of genetic factors and chronic exposure to a high-iodine diet. The mean age at diagnosis is 60 years, and the prevalence of overt hypothyroidism increases with age. Subclinical hypothyroidism is found in 6–8% of women (10% over the age of 60) and 3% of men. The annual risk of developing clinical hypothyroidism is about 4%.A high iodine intake and decreased exposure to microorganisms in childhood increase the risk of autoimmune hypothyroidism. These factors may account for the increase in prevalence over the last two to three decades.
Thyroid-associated ophthalmopathy, which usually occurs in Graves’ disease, occurs in about 5% of patients with autoimmune hypothyroidism. Autoimmune hypothyroidism is uncommon in children and usually presents with slow growth and delayed facial maturation. The appearance of permanent teeth is also delayed. Myopathy, with muscle swelling, is more common in children than in adults. In most cases, puberty is delayed, but precocious puberty sometimes occurs. There may be intellectual impairment if the onset is before 3 years and the hormone deficiency is severe.
FNA biopsy can be used to confirm the presence of autoimmune thyroiditis. Other abnormal laboratory findings in hypothyroidism may include increased creatine phosphokinase, elevated cholesterol and triglycerides, and anemia (usually normocytic or macrocytic)
Iatrogenic hypothyroidism is a common cause of hypothyroidism and can often be detected by screening before symptoms develop.
Paradoxically, chronic iodine excess can also induce goiter and hypothyroidism. The intracellular events that account for this effect are unclear, but individuals with autoimmune thyroiditis are especially susceptible. Iodine excess is responsible for the hypothyroidism that occurs in up to 13% of patients. Other drugs, particularly lithium, may also cause hypothyroidism.
Secondary hypothyroidism diagnosis is confirmed by detecting a low unbound T4 level.
By definition, subclinical hypothyroidism refers to biochemical evidence of thyroid hormone deficiency in patients who have few or no apparent clinical features of hypothyroidism.
It is important to confirm that any elevation of TSH is sustained over a 3-month period before treatment is given. As long as excessive treatment is avoided, there is no risk in correcting a slightly increased TSH.
Women with a history or high risk of hypothyroidism should ensure that they are euthyroid prior to conception and during early pregnancy because maternal hypothyroidism may adversely affect fetal neural development and cause preterm delivery. The presence of thyroid autoantibodies alone, in a euthyroid patient, is also associated with miscarriage and preterm delivery. Thyroid function should be evaluated immediately after pregnancy is confirmed and every 4 weeks during the first half of the pregnancy, with less frequent testing after 20 weeks’ gestation.
Clinical manifestations include reduced level of consciousness, sometimes associated with seizures, as well as the other features of hypothyroidism (Table 405-6). Hypothermia can reach 23°C (74°F). There may be a history of treated hypothyroidism with poor compliance, or the patient may be previously undiagnosed.
The metabolism of most medications is impaired, and sedatives should be avoided if possible or used in reduced doses. Medication blood levels should be monitored, when available, to guide dosage.
Rectum complaints
HAEMORRHOIDS
Hemorrhoids are dilated veins within the anal canal in the sub epithelial region form the radical of the superior middle and inferior rectal vein.
TYPES OF HEMORRHOIDS:
1. External hemorrhoids: Situated outside the anal orifice and covered by the skin.
2. Internal hemorrhoids:
Within the anal canal and internal to the anal orifice. Each primary internal hemorrhoids contains main terminal division of superior rectal vessels arranged in the left lateral, right anterior and right posterior positions. In lithotomy position these correspond with the 3, 7 and 11 O’ clock positions.
RISK FACTOR:
Dietary habits
• Low fibre diet
• Mixed diet
• Poor hydration
Bowel habits
• Chronic constipation
• Diarrhoea
• Straining during defecation
Amount of physical activity
• Low physical activity
Obesity
Pregnancy
Sedentary lifestyle
Habit of postponing the bowel movements,
Spinal cord injuries.
CLINICAL FEATURES:
1. BLEEDING
2. PROLAPSE: hemorrhoids are further graded based on their appearance and degree of prolapse:
Grade I: Non-prolapsing hemorrhoids;
Grade II: Prolapsing hemorrhoids on straining but reduce spontaneously;
Grade III: Prolapsing hemorrhoids requiring manual reduction; and
Grade IV: Non-reducible prolapsing hemorrhoids which include acutely thrombosed, incarcerated hemorrhoids.
3. MUCUS DISCHARGE
4. ANEMIA
5. PAIN
INVESTIGATION
• INSPECTION
Internal haemorrhoids without prolapse will not show any abnormal features. In fourth degree the prolapsed piles can be seen in 3, 7 and 11 O’clock position.
• DIGITAL EXAMINATION
Cannot feel an uncomplicated internal piles unless it is thrombosed
• PROCTOSCOPY
A proctoscope is passed to its fullest extend and the obturator is removed. The instrument is then slowly withdrawn. Just below the anorectal ring internal haemorrhoid if present will bulge into the lumen of the proctoscope.
COMPLICATION
• Excessive bleeding
• Thrombosis
• Ulceration
• Fibrosis
• Strangulation
• Gangrene
• Infection and suppuration
• Pylophlebitis and portal pyaemia - very rare
TREATMENT[8]
Treatment options mainly depend on the type and severity of hemorrhoids, patient’s preference, and the expertise of physicians. The current therapies can be grouped into
• CONSERVATIVE MANAGEMENT: Increased fiber intake, medical therapies, and lifestyle changes are included in the conservative treatment options for non-thrombosed hemorrhoids
• OFFICE-BASED PROCEDURES: Rubber-band ligation, injection sclerotherapy, laser photocoagulation, bipolar diathermy, cryotherapy, Doppler-guided hemorrhoidal artery ligation and infrared coagulation; still, they are not suitable for all grades of hemorrhoids and have recognized complications.
• SURGICAL TREATMENT: Hemorrhoidectomy, thrombectomy of external hemorrhoids, and stapled hemorrhoidectomy; however, no single technique has been universally accepted as superior.
Based on clinical practice, it is assumed that surgery is effective for severe prolapsing hemorrhoids, but it is difficult to deal with the post-operative complications. Thus, controversies and lack of agreement still exist on treatment strategies.
Homeopathic literature shows anecdotal data on the usefulness of homeopathic medicines in hemorrhoids. Although remarkable cure of hemorrhoids with homeopathic medicines in casual clinical experiences has been noted, research evidence remains seriously compromised.
ANAL FISSURE
Anal fissures occur at all ages but are more common in the third through the fifth decades. A fissure is the most common cause of rectal bleeding in infancy. The prevalence is equal in males and females. It is associated with constipation, diarrhea, infectious etiologies, perianal trauma, and Crohn’s disease.
Trauma to the anal canal occurs following defecation. This injury occurs in the anterior or, more commonly, the posterior anal canal. Irritation caused by the trauma to the anal canal results in an increased resting pressure of the internal sphincter. The blood supply to the sphincter and anal mucosa enters laterally. Therefore, increased anal sphincter tone results in a relative ischemia in the region of the fissure and leads to poor healing of the anal injury. A fissure that is not in the posterior or anterior position should raise suspicion for other causes, including tuberculosis, syphilis, Crohn’s disease, and malignancy.
A fissure can be easily diagnosed on history alone. The classic complaint is pain, which is strongly associated with defecation and is relentless. The bright red bleeding that can be associated with a fissure is less extensive than that associated with hemorrhoids. On examination, most fissures are located in either the posterior or anterior position. A lateral fissure is worrisome because it may have a less benign nature, and systemic disorders should be ruled out. A chronic fissure is indicated by the presence of a hypertrophied anal papilla at the proximal end of the fissure and a sentinel pile or skin tag at the distal end. Often the circular fibers of the hypertrophied internal sphincter are visible within the base of the fissure. If anal manometry is performed, elevation in anal resting pressure and a sawtooth deformity with paradoxical contractions of the sphincter muscles are pathognomonic. The management of the acute fissure is conservative. Stool softeners for those with constipation, increased dietary fiber and sitz baths are prescribed and will heal 60–90% of fissures. Chronic fissures are those present for >6 weeks.
FISTULA-IN-ANO
Fistula-in-ano is an inflammatory track which has an external opening (secondary opening) in the perianal skin and an internal opening (primary opening) in the anal canal or rectum. This track is lined by unhealthy granulation tissue and fibrous tissue.
The fistula usually originates from a perianal abscess ip the intersphincteric space of the anal canal from infection of the anal gland. As the anal gland is situated deep to the internal sphincter its duct passes through the internal sphincter to open in the crypts of Morgagni situated on the dentate line. Due to the tone the internal sphincter the duct cannot aptly discharge the contents of the gland. Stasis and secondary infection lead to abscess formation from the anal gland in the intersphincteric region. From here the internal opening
traverse through the internal sphincter to open into the anal canal and the abscess usually tracks down and in the perianal skin externally thus fistula-in-ano is formed. Several other disorders must be considered which may cause fistula-in-ano. These are :
(b) Ulcerative colitis, (c) Crohn’s disease, (d) Tuberculosis and (e) Colloid carcinoma of the rectum.
CLASSIFICATION.— Broadly, anal fistula can be divided into two groups — (I) low fistula and (II) high fistula depending on whether the internal opening is below or above the anorectal ring respectively.
(I) Low level fistula.— These fistulae open into the anal canal below the anorectal ring. These can be further subdivided into (i) subcutaneous type, (ii) submucous type, (iii) intersphincteric type, (iv) transphincteric type and (v) suprasphincteric type.
(II) High level fistula.— These fistulae open into the anal canal at or above the anorectal ring. These can be further subdivided into (i) extrasphincteric or supralevator type, (ii) transphincteric type (which
may be seen in low variety also) and (iii) pelvi-rectal fistula. The importance of deciding whether a fistula is a low or a high level type is that a low level fistula can be laid open without fear of permanent incontinence as the anorectal ring
Whereas in case of high level fistula one must diagnose the case before operation and it is usually treated by stages, lest damage to the anorectal ring may cause permanent incontinence.
A fistula may be single or multiple. When there is more than one external opening it is called a multiple anal fistula. In this case there may be one or more internal openings.
Clinical features.— Usually a past history of perianal abscess can be received. The abscess formed and ruptured by itself, the condition healed leaving a tiny discharging sinus. After a few month, again abscess formed, ruptured by itself and a discharging opening is left. After a few recurrent attacks the discharging fistula fails to heal and continues to discharge. This condition also develops when after abscess formation an inadequate incision is made for drainage. Similarly new abscesses may form to cause multiple fistulae.
Tuberculosis is a very common cause of multiple fistulae in this country. More common is solitary fistula with an external opening within 3.7 cm of the anus. Granulation tissue may be seen pouting out from the mouth the fistula. There is much induration of the skin and subcutaneous tissue around the fistula. When fistula forms
secondary to ischiorectal abscess, both the ischiorectal fossae may be involved. An external opening for each side of the ischiorectal fossa may be seen with intercommunicating track lying posterior to the anus. This is called horse-shoe fistula.
GOODSALL'S RULE.— This rule relates the location of the internal opening to the external opening. If the external opening is anterior to an imaginary line drawn-across the midpoint of the anus, the fistula runs straight directly into the anal canal. If the external opening is situated posterior to that line, the track usually curve and the internal opening will be on the midline posterior of the anal canal. An exception to this rule is the external opening is anterior to this imaginary line but is situated more than 1V2 inches (3.75 cm) away from the anus. In this case the track will curve posteriorly and end in the posterior midline.
The internal opening must be felt by digital examination. If it is above the anorectal ring it is a high fistula and the treatment is different from low fistula. Number of internal openings must be noted. Even if there are multiple external fistulae there may be one internal opening.
PROCTOSCOPY — is sometimes necessary to visualise internal opening of the fistula.
LIPIODOL INJECTION—into the eternal opening prior to radiography will show the track of fistula-in-ano. But its utility is in doubt as it seldom gives more information and on the contrary it causes a recrudescence of inflammation.
CHEST X-RAY to exclude tuberculosis is important as fistula-in-ano is often associated with tuberculosis in this country. If the surrounding skin of the fistula is discoloured and the discharge is watery, it strongly suggests a tuberculous origin. In this case, induration around the Fistula is lacking and the opening is irregular with undermined edge. If any doubt regarding cause of fistula-in-ano, the following conditions must be excluded. These are : (a) Tuberculous proctitis, (b) Ulcerative colitis, (c) Crohn’s disease, (d) Bilharziasis, (e) Lymphogranuloma inguinale and (f) Colloid carcinoma of the rectum.
TREATMENT
LOW level fistula.—Fistula track must be laid open. The patient is placed in lithotomy position. The bidigital examination is made under anaesthesia to reveal cord like induration representing the track. A probe is inserted through the Fistula track. Care must be taken not to create a false passage. A propointed director is now introduced through the external opening and its tip comes out through the internal opening. With a knife the track is now opened on the director. If there are multiple fistulae the probe-pointed director is passed through
individual external opening and brought out through the internal opening and the corresponding track is laid open with the knife. After the Fistula track has been laid open, (i) either the unhealthy granulation tissue on the wall of the fistula is scraped off with a Volkmann spoon or (ii) the whole track with the fibrous tissue is excised. The cavity is packed with roller gauze wrung with weak antiseptic lotion. Healing will take place by granulation
tissue from the depth. Some surgeons have advocated split skin graft of the wound resulting from fistulotomy. The grafts are taken
from the inner aspect of the thigh and applied to the anal wound by stitching to the skin edges. However this is not advised as a routine practice.
High level fistula.—
(i) Supralevator fistula is mostly secondary to Crohn’s disease or ulcerative colitis or carcinoma or foreign body. This requires treatment of the primary condition and the fistula is ignored. Any attempt to lay open the fistula will cause incontinence.
(ii) Transphincteric fistula with a perforating secondary track.— In this case there is almost always a low fistula and if care is not taken while inserting the probe-pointed director, the director will go into the high secondary track and if passed hard will open into the rectum above the anorectal ring transforming the condition into a high fistula. So in this type of fistula the lower track is opened as usual and the upper track opening is made wide with scraping the high fistula with Volkmann spoon. The upper track will heal by itself alongwith the low fistula. Alternatively the lower part of the track is treated by Fistulotomy. Then a seton of heavy black silk or a rubber band is passed round the deeper part of the track. This will include intact fibres of the sphincter and the anal canal mucous membrane. The silk is tied loosely outside and kept in situ for two weeks. This stimulates fibrosis adjacent to the sphincter muscle. In the second stage, after 6 weeks, the remaining part of the track including the fibres of the sphincter muscles incorporated within the tie is excised. Fibrosis, from the previous operation, prevents retraction of the freshly cut sphincteric fibres. So incontinence which is the most serious complication of this operation is avoided. This operation is known as Gabriel's two-stage operation. Instead of passing the silk, a stainless steel wire may be passed round the deeper part of the track. After two weeks, the knot is gradually tightened during subsequent dressings. The wire cuts through the shows use of Seton in case of high fistula. Healing occurs in parts as the new portion is cut and the old portion (iii) High intersphincteric fistula.— It is also treated in the similar fashion as described in the previous section.
Horse-shoe fistula is usually not treated by radical unroofing procedure (fistulotomy). Instead a posterior midline internal sphincterotomy combined with laying open the deep part of the fistula track is performed. lateral tracks are excised. This has proved effective. This is Wanley operation.
Kidney stone
A stone may form due to crystallization of lithogenic factors in the upper urinary tract, it can subsequently move into the ureter and cause renal colic. Although kidney stone is rarely fatal, patients who have had renal colic report that it is the worst pain they have ever experienced.
There are various types of kidney stones. It is clinically important to identify the stone type, which informs prognosis and selection of the optimal preventive regimen. Calcium oxalate stones are most common (~75%); next, in order, are calcium phosphate (~15%), uric acid (~8%), struvite (~1%), and cystine (<1%) stones. Many stones are a mixture of crystal types (e.g., calcium oxalate and calcium phosphate) and also contain protein in the stone matrix. Rarely, stones are composed of medications, such as acyclovir, indinavir, and triamterene. Infectious stones, if not appropriately treated, can have devastating consequences and lead to end-stage renal disease.
Nephrolithiasis is a global disease likely due to Westernization of lifestyle habits (e.g., dietary changes, increasing body mass index).Once an individual has had a stone, the prevention of a recurrence is essential. Most experts agree that radiographic evidence of a second stone should be considered to represent a recurrence, even if the stone has not yet caused symptoms.
Risk factors for nephrolithiasis can be categorized as dietary, nondietary, or urinary. Efforts to avoid high oxalate intake, higher intake of animal protein, higher sodium and sucrose intake should be beneficial. Avoidance of foods that contain high amounts of oxalate, such as spinach, rhubarb, and potatoes, is prudent. Calcium oxalate stone formers should be advised to avoid vitamin C supplements. The risk of stone formation increases as urine volume decreases. When the urine output is less than 1 L/d, the risk of stone formation more than doubles. Fluid intake is the main determinant of urine volume. Coffee, tea, beer, and wine are associated with a reduced risk of stone formation. Sugar-sweetened carbonated beverage consumption may increase risk.
The incidence of stone disease is highest in middle-aged white men, but stones can form in infants as well as in the elderly. Weight gain increases the risk of stone formation, Environmental and occupational influences that may lead to lower urine volume, such as working in a hot environment or lack of ready access to water or a bathroom, are important considerations.
Urine pH influences the solubility of some crystal types. Uric acid stones form only when the urine pH is consistently ≤5.5 or lower, whereas calcium phosphate stones are more likely to form when the urine pH is ≥6.5 or higher. Cystine is more soluble at higher urine pH. Calcium oxalate stones are not influenced by urine pH.
The risk of nephrolithiasis is more than twofold greater in individuals with a family history of stone disease. This association is likely due to a combination of genetic predisposition and similar environmental exposures.
It typically requires weeks to months (and often much longer) for a kidney stone to grow to a clinically detectable size. Although the passage of a stone is a dramatic event, stone formation and growth are characteristically clinically silent. A stone can remain asymptomatic in the kidney for years or even decades before signs (e.g., hematuria) or symptoms (e.g., pain) become apparent. Thus, it is important to remember that the onset of symptoms, typically attributable to a stone moving into the ureter, does not provide insight into when the stone actually formed.
There are two common presentations for individuals with an acute stone event: renal colic and painless gross hematuria.
Renal colic is a misnomer because pain typically does not subside completely; rather, it varies in intensity. When a stone moves into the ureter, the discomfort often begins with a sudden onset of unilateral flank pain. The intensity of the pain can increase rapidly, and there are no alleviating factors. This pain, which is accompanied often by nausea and occasionally by vomiting, may radiate, depending on the location of the stone. If the stone lodges in the upper part of the ureter, pain may radiate anteriorly; if the stone is in the lower part of the ureter, pain can radiate to the ipsilateral testicle in men or the ipsilateral labium in women. Occasionally, a patient has gross hematuria without pain.
The urine will contain red and white blood cells, but the urine culture will be negative. An obstructing stone with proximal infection may present as acute pyelonephritis.
The diagnosis is often made on the basis of the history, physical examination, and urinalysis. Thus, it may not be necessary to wait for radiographic confirmation before treating the symptoms. Helical CT detects stones as small as 1 mm that may be missed by other imaging modalities. Typically, helical CT reveals a ureteral stone or evidence of recent passage (e.g., perinephric stranding or hydronephrosis), whereas a plain abdominal radiograph (kidney/ureter/bladder, or KUB) can miss a stone in the ureter or kidney, even if it is radiopaque, and does not provide information on obstruction. Abdominal ultrasound offers the advantage of avoiding radiation and provides information on hydronephrosis, but it is not as sensitive as CT and images only the kidney and possibly the proximal segment of the ureter; thus most ureteral stones are not detectable by ultrasound. Excessive fluid administration has not been shown to be beneficial; therefore, the goal should be to maintain euvolemia.
The urine volume should be at least 2 L/d. Because of differences in insensible fluid losses and fluid intake from food sources, the required total fluid intake will vary from person to person. Rather than specify how much to drink, it is more helpful to educate patients about how much more they need to drink in light of their 24-h urine volume. For example, if the daily urine volume is 1.5 L, then the patient should be advised to drink at least 0.5 L more per day in order to increase the urine volume to the goal of 2 L/day.
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