MANEGEMENT OF AMENORRHEA ACCORDING TO AYURVED AND MODERN SCIENCE

INTRODUCTION

Amenorrhoea is the absence of a menstrual period in a woman of reproductive age. Physiological states of amenorrhoea are seen, most commonly, during pregnancy and lactation, the latter also forming the basis of a form of contraception known as the lactation amenorrhoea method. Outside of the reproductive years there is absence of menses during childhood and after menopause.

Amenorrhoea is a symptom with many potential causes. Primary amenorrhoea (menstruation cycles never starting) may be caused by developmental problems such as the congenital absence of the uterus, failure of the ovary to receive or maintain egg cells. Also, delay in pubertal development will lead to primary amenorrhoea. It is defined as an absence of secondary sexual characteristics by age 14 with no menarche or normal secondary sexual characteristics but no menarche by 16 years of age. Secondary amenorrhoea (menstruation cycles ceasing) is often caused by hormonal disturbances from the hypothalamus and the pituitary gland, from premature menopause or intrauterine scar formation. It is defined as the absence of menses for three months in a woman with previously normal menstruation or nine months for women with a history of oligomenorrhoea

Classification

There are two primary ways to classify amenorrhoea. Types of amenorrhoea are classified as primary or secondary, or based on functional "compartments". The latter classification relates to the hormonal state of the patient that hypo-, eu-, or hypergonadotropic (whereby interruption to the communication between gonads and follicle stimulating hormone (FSH) causes FSH levels to be either low, normal or high).

• Primary amenorrhoea is the absence of menstruation in a woman by the age of 16. As pubertal changes precede the first period, or menarche, women by the age of 14 who still have not reached menarche, plus having no sign of secondary sexual characteristics, such as thelarche or pubarche—thus are without evidence of initiation of puberty—are also considered as having primary amenorrhoea. Secondary amenorrhoea is where an established menstruation has ceased—for three months in a woman with a history of regular cyclic bleeding, or nine months in a woman with a history of irregular periods. This usually happens to women aged 40–55. However, adolescent athletes are more likely to experience disturbances to the menstrual cycle than athletes of any other age.[5] Amenorrhoea may cause serious pain in the back near the pelvis and spine. This pain has no cure, but can be relieved by a short course of progesterone to trigger menstrual bleeding.

•             By compartment: The reproductive axis can be viewed as having four compartments:

1. Outflow tract (uterus, cervix, and vagina),

2. Ovaries,

 3. Pituitary gland, and

 4. Hypothalamus.

Pituitary and hypothalamic causes are often grouped together Primary/Secondary          Outflow tract anomalies/obstruction  Gonadal/end-organ disorders    Pituitary and hypothalamic/central regulatory disorders

Overview            The hypothalamic-pituitary-ovarian axis is functional.     The ovary or gonad does not respond to pituitary stimulation. Gonadal dysgenesis or premature menopause are possible causes.Chromosome testing is usually indicated in younger individuals with hypergonadotropic amenorrhoea. Low oestrogen levels are seen in these patients and the hypo-oestrogenism may require treatment.   Generally, inadequate levels of FSH lead to inadequately stimulated ovaries which then fail to produce enough oestrogen to stimulate theendometrium (uterine lining), hence amenorrhoea. In general, women with hypogonadotropic amenorrhoea are potentially fertile.

FSH

Outflow tract abnormalities tend to be normogonadotropic and FSH levels are in the normal range.         Gonadal, usually ovarian, abnormalities tend to be linked to elevated FSH levels or hypergonadotropic amenorrhoea. FSH levels are typically in the menopausal range.            Both hypothalamic and pituitary disorders are linked to low FSH levels leading to hypogonadotropic amenorrhoea.

Primary

                •             Uterine: Müllerian agenesis (Second most common cause, 15% of primary amenorrhoea)

•             Vaginal: Vaginal atresia, cryptomenorrhoea, imperforate hymen.

•             Gonadal  dysgenesis, including Turner syndrome, is the most common cause.

•             Androgen insensitivity syndrome (Testicular feminization syndrome)

•             Receptor abnormalities for hormones FSH and LH

•             Specific forms of congenital adrenal hyperplasia

•             Swyer syndrome

•             Galactosaemia

•             Aromatase deficiency

•             Prader-Willi syndrome

•             Male pseudo-hermaphroditism (about 1 in every 150,000 births)

•             Müllerian agenesis/MRKH Syndrome

•             Other intersexed conditions

                •             hypothalamic: Kallmann syndrome

Secondary          

•             Intrauterine adhesions (Asherman's syndrome)

•             Pregnancy (most common cause)

•             Anovulation

•             Menopause

•             Premature menopause

•             Polycystic ovary syndrome

•             Drug-induced

•             Breastfeeding

•             Hypothalamic: Exercise amenorrhoea, related tophysical exercise, stress amenorrhoea, eating disorders and weight loss (obesity, anorexia nervosa, or bulimia)

•             Pituitary: Sheehan syndrome, hyperprolactinaemia,haemochromatosis

•             Other central regulatory: hypothyroidism, hyperthyroidism, arrhenoblastoma

Cause Low body weight

Women who perform considerable amounts of exercise on a regular basis or lose a significant amount of weight are at risk of developing hypothalamic (or 'athletic') amenorrhoea. Functional Hypothalamic Amenorrhoea (FHA) can be caused by stress, weight loss, and/or excessive exercise. Many women who diet or who exercise at a high level do not take in enough calories to expend on their exercise as well as to maintain their normal menstrual cycles. The threshold of developing amenorrhoea appears to be dependent on low energy availability rather than absolute weight because a critical minimum amount of stored, easily mobilized energy is necessary to maintain regular menstrual cycles.

Energy imbalance and weight loss can disrupt menstrual cycles through several hormonal mechanisms. Weight loss can cause elevations in the hormone ghrelin which inhibits the hypothalamic-pituitary-ovarial axis.[9] Elevated concentrations of ghrelin alter the amplitude of GnRH pulses, which causes diminished pituitary release of LH and follicle-stimulating hormone (FSH).

Secondary amenorrhea is caused by low levels of the hormone leptin in females with low body weight.  Like ghrelin, leptin signals energy balance and fat stores to the reproductive axis. Decreased levels of leptin are closely related to low levels of body fat, and correlate with a slowing of GnRH pulsing.

When a woman is experiencing amenorrhoea, an eating disorder, and osteoporosis together, this is called female athlete triad syndrome. A lack of eating causes amenorrhoea and bone loss leading to osteopenia and sometimes progressing to osteoporosis.[citation needed]

The social effects of amenorrhoea on a person vary significantly. Amenorrhoea is often associated with anorexia nervosa and other eating disorders, which have their own effects. If secondary amenorrhoea is triggered early in life, for example through excessive exercise or weight loss, menarche may not return later in life. A woman in this situation may be unable to become pregnant, even with the help of drugs. Long-term amenorrhoea leads to an estrogens deficiency which can bring about menopause at an early age. The hormone oestrogen plays a significant role in regulating calcium loss after ages 25–30. When her ovaries no longer produce oestrogen because of amenorrhoea, a woman is more likely to suffer rapid calcium loss, which in turn can lead to osteoporosis. Increased testosterone levels cause by amenorrhoea may lead to body hair growth and decreased breast size. Increased levels of androgens, especially testosterone, can also lead to ovarian cysts. Some research among amenorrhoea runners indicates that the loss of menses may be accompanied by a loss of self-esteem.

Drug-induced

Certain medications, particularly contraceptive medications, can induce amenorrhoea in a healthy woman. The lack of menstruation usually begins shortly after beginning the medication and can take up to a year to resume after stopping a medication. Hormonal contraceptives that contain only progestogen like the oral contraceptive Micronor, and especially higher-dose formulations like the injectable Depo Provera commonly induce this side-effect. Extended cycle use of combined hormonal contraceptives also allow suppression of menstruation. Patients who use and then cease using contraceptives like the combined oral contraceptive pill may experience secondary amenorrhoea as a withdrawal symptom. The link is not well understood, as studies have found no difference in hormone levels between women who develop amenorrhoea as a withdrawal symptom following the cessation of OCOP use and women who experience secondary amenorrhoea because of other reasons. New contraceptive pills, like continuous oral contraceptive pills (OCPs) which do not have the normal 7 days of placebo pills in each cycle, have been shown to increase rates of amenorrhoea in women. Studies show that women are most likely to experience amenorrhoea after 1 year of treatment with continuous OCP use.

The use of opiates (such as heroin) on a regular basis has also been known to cause amenorrhoea in longer term users.[citation needed]

Anti-psychotic drugs used to treat schizophrenia have been known to cause amenorrhoea as well. New research suggests that adding a dosage of Metformin to an anti-psychotic drug regimen can restore menstruation. Metformin decreases resistance to the hormone insulin, as well as levels of prolactin, testosterone, and lutenizing hormone (LH). Metformin also decreases the LH/FSH ratio. Results of the study on Metformin further implicate the regulation of these hormones as a main cause of secondary amenorrhoea.

Breastfeeding

Breastfeeding is a common cause of secondary amenorrhoea, and often the condition lasts for over six months.[20] Breastfeeding typically lasts longer than lactational amenorrhoea, and the duration of amenorrhoea varies depending on how often a women breastfeeds. Lactational amenorrhoea has been advocated as a method of family planning, especially in developing countries where access to other methods of contraception may be limited. Breastfeeding is said to prevent more births in the developing world than any other method of birth control or contraception. Lactational amenorrhoea is 98% percent effective as a method of preventing pregnancy in the first six months postpartum.

Physical

Amenorrhoea can also be caused by physical deformities. One example of this is Mayer–Rokitansky–Küster–Hauser syndrome, the second-most common cause of primary amenorrhoea. The syndrome is characterized by Müllerian agenesis. In MRKH Syndrome, the Müllerian ducts do not develop, which prevents menstruation. The syndrome usually develops during the first trimester of pregnancy. MRI techniques can be helpful in determining the extent of the problem. Women may recover from MRKH syndrome, but other times primary amenorrhoea, which is characteristic of the disorder, may prevent pregnancy for life.

DiagnosisPrimary amenorrhoea

Primary amenorrhoea can be diagnosed in women by age 14 if no secondary sex characteristics, such as enlarged breasts and body hair, are present In the absence of secondary sex characteristics, the most common cause of amenorrhoea is low levels of FSH and LH caused by a delay in puberty. Gonadal dysgenesis, often associated withTurner's Syndrome, or premature ovarian failure may also be to blame. If secondary sex characteristics are present, but menstruation is not, primary amenorrhoea can be diagnosed by age 16. A reason for this occurrence may be that a person phenotypically female but genetically male, a situation known as androgen insensitivity syndrome. If undescended testes are present, they are often removed after puberty (~21 years of age) due to the increased risk of testicular cancer. In the absence of undescended testes, an MRI can be used to determine whether or not a uterus is present. Müllerian agenesis causes around 15% of primary amenorrhoea cases. If a uterus is present, outflow track obstruction may be to blame for primary amenorrhoea.

Secondary amenorrhea

Secondary amenorrhea's most common and most easily diagnosable causes are pregnancy, thyroid disease, and hyperprolactinemia. A pregnancy test is a common first step for diagnosis.[Hyperprolactinemia, characterized by high levels of the hormone prolactin, is often associated with a pituitary tumor. A dopamine agonist can often help relieve symptoms. The subsiding of the causal syndrome is usually enough to restore menses after a few months. Secondary amenorrhea may also be caused by outflow tract obstruction, often related to Asherman's Syndrome. Polycystic ovary syndrome can cause secondary amenorrhea, although the link between the two is not well understood. Ovarian failure related to early onset menopause can cause secondary amenorrhea, and although the condition can usually be treated, it is not always reversible. Secondary amenorrhea is also caused by stress, extreme weight loss, and excessive exercise. Young athletes are particularly vulnerable, although normal menses usually return with healthy body weight. Causes of secondary amenorrhea can also result in primary amenorrhea, especially if present before onset of menarche.

Treatments

Treatments vary based on the underlying condition. Key issues are problems of surgical correction if appropriate and oestrogen therapy if oestrogen levels are low. For those who do not plan to have biological children, treatment may be unnecessary if the underlying cause of the amenorrhoea is not threatening to their health. However, in the case of athletic amenorrhoea, deficiencies in estrogen and leptin often simultaneously result in bone loss, potentially leading to osteoporosis.

"Athletic" amenorrhoea which is part of the female athlete triad is treated by eating more and decreasing the amount and intensity of exercise. If the underlying cause is the athlete triad then a multidisciplinary treatment including monitoring from a physician, dietitian, and mental health counselor is recommended, along with support from family, friends, and coaches. Although oral contraceptives can causes menses to return, oral contraceptives should not be the initial treatment as they can mask the underlying problem and allow other effects of the eating disorder, like osteoporosis, continue to develop. Weight recovery, or increased rest does not always catalyze the return of a menses. Recommencement of ovulation suggests a dependency on a whole network of neurotransmitters and hormones, altered in response to the initial triggers of secondary amenorrhoea. To treat drug-induced amenorrhoea, stopping the medication on the advice of a doctor is a usual course of action.

Looking at Hypothalamic amenorrhoea, studies have provided that the administration of a selective serotonin reuptake inhibitor (SSRI) might correct abnormalities of Functional Hypothalamic Amenorrhoea (FHA) related to the condition of stress-related amenorrhoea. This involves the repair of the PI3K signaling pathway, which facilitates the integration of metabolic and neural signals regulating gonadotropin releasing hormone (GnRH)/luteinizing hormone (LH). In other words, it regulates the neuronal activity and expression of neuropeptide systems that promote GnRH release. However, SSRI therapy represents a possible hormonal solution to just one hormonal condition of hypothalamic amenorrhoea. Furthermore, because the condition involves the inter workings of many different neurotransmitters, much research is still to be done on presenting hormonal treatment that would counteract the hormonal affects.

As for physiological treatments to hypothalamic amenorrhoea, injections of metreleptin (r-metHuLeptin) have been tested as treatment to oestrogen deficiency resulting from low gonadotropins and other neuroendocrine defects such as low concentrations of thyroid and IGF-1. R-metHuLeptin has appeared effective in restoring defects in the hypothalamic-pituitary-gonadal axis and improving reproductive, thyroid, and IGF hormones, as well as bone formation, thus curing the amenorrhoea and infertility. However, it has not proved effective in restoring of cortisol and adrenocorticotropin levels, or bone resorption

Ayurvedic treatment

1-the use of bastis is beneficial.

2-fish kulattha,sour substances (kanji),tail,mamsa , wine ,urine(cow urine), butter-milk mixed with half water, curd and sukta should be used in diet and drinks

3-in all disorders  of artava use of lasuna , satpushpa and  satavari is beneficial.

4-A pessary made with powdered seed of ikswaku,danti,capala,jiggery,madanphla ,kinva and yavasuka triturated with latex of snuhi should be placed in yoni(cervix).this induces menstruation.

5-use of powdered leaves of jyotismati, swarjikasara or rajika ugra and steam bark of asana with cold water for three days induces menstruation positively

6-use of satawaryadi anuwasana basti is beneficial

AYURVEDIC FORMULATIONS 

1 Phalaghrata

2-Vrhatsatavari ghrta

3-Arogya vardhini vati

4- Rajaha pravartini vati

5-Dashmularista

6-Rkata pachak kwath

7-Rashpachak kwath

Stevens–Johnson syndrome (SJS

Stevens–Johnson syndrome (SJS) is a type of severe skin reaction. Together with toxic epidermal necrolysis (TEN) it forms a spectrum of disease, with SJS being less severe. Early symptoms include fever and flu-like symptoms.

 A few days later the skin begins to blister and peel forming painful raw areas. Mucous membranes, such as the mouth, are also typically involved. Complications include dehydration, sepsis, pneumonia, and multiple organ failure.

The most common cause is certain medications such as 

1-lamotrigine,

2-carbamazepine,

3-allopurinol,

4-sulphonamide

 5-antibiotics,

6- nevirapine.

Other causes can include infections such as Mycoplasma pneumoniae and cytomegalovirus or the cause may remain unknown. Risk factors include HIV/AIDS and systemic lupus erythematosus. The diagnosis is based on involvement of less than 10% of the skin. It is known as TEN when more than 30% of the skin is involved and an intermediate form with 10 to 30% involvement. Erythema multiform (EM) is generally considered a separate condition.

Treatment -

v Treatment typically takes place in hospital such as in a burn unit or intensive care unit. Efforts may include stopping the cause, pain medication, antihistamines, antibiotics, intravenous immunoglobulins, or corticosteroids.

v Together with TEN it affects 1 to 2 people per million per year.

v It is twice as common in males as females. Typical onset is under the age of 30. Skin usually regrows over two to three weeks; however, complete recovery can take months.

v Signs and symptoms

v Mucosal desquamation in a person with Stevens–Johnson syndrome.

v Conjunctivitis (inflammation of eye and eyelid) in SJS

v SJS usually begins with fever, sore throat, and fatigue, which is commonly misdiagnosed and therefore treated with antibiotics. SJS and TEN are often heralded by fever, sore throat, cough, and burning eyes for 1 to 3 days. Patients with SJS and TEN frequently experience burning pain of their skin at the start of disease. Ulcers and other lesions begin to appear in the mucous membranes, almost always in the mouth and lips, but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient's ability to eat or drink. Conjunctivitis of the eyes occurs in about 30% of children who develop SJS.[medical citation needed] A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet, but usually not the scalp.

Causes

SJS is thought to arise from a disorder of the immune system. The immune reaction can be triggered by drugs or infections. Genetic factors are associated with a predisposition to SJS. The cause of SJS is unknown in one-quarter to one-half of cases. SJS and TEN are considered a single disease with common causes and mechanisms.

Medication

Although SJS can be caused by viral infections and malignancies, the main cause is medications. A leading cause appears to be the use of antibiotics, particularly sulfa drugs. Between 100 and 200 different drugs may be associated with SJS. No reliable test exists to establish a link between a particular drug and SJS for an individual case. Determining what drug is the cause is based on the time interval between first use of the drug and the beginning of the skin reaction. Drugs discontinued more than 1 month prior to onset of mucocutaneous physical findings are highly unlikely to cause SJS and TEN. SJS and TEN most often begin between 4 and 28 days after culprit drug administration. A published algorithm (ALDEN) to assess drug causality gives structured assistance in identifying the responsible medication.

v SJS may be caused by adverse effects of the drugs vancomycin,

Ø allopurinol,

Ø valproate,

Ø levofloxacin,

Ø diclofenac,

Ø etravirine,

Ø isotretinoin,

Ø fluconazole,

Ø valdecoxib,

Ø sitagliptin,

Ø oseltamivir,

Ø penicillins,

Ø barbiturates,

Ø sulfonamides,

Ø phenytoin,

Ø azithromycin,

Ø oxcarbazepine,

Ø zonisamide,

Ø modafinil,

Ø lamotrigine,

Ø nevirapine,

Ø pyrimethamine,

Ø ibuprofen,

Ø carbamazepine,

Ø bupropion,

Ø telaprevir,and nystatin.

Medications that have traditionally been known to lead to SJS, erythema multiforme, and toxic epidermal necrolysis include sulfonamideantibiotics, penicillin antibiotics, cefixime (antibiotic), barbiturates (sedatives), lamotrigine, phenytoin (e.g., Dilantin) (anticonvulsants) and trimethoprim. Combining lamotrigine with sodium valproate increases the risk of SJS.

Ø Nonsteroidal anti-inflammatory drugs (NSAIDs) are a rare cause of SJS in adults; the risk is higher for older patients, women, and those initiating treatment.Typically, the symptoms of drug-induced SJS arise within a week of starting the medication. Similar to NSAIDs, paracetamol (acetaminophen) has also caused rare cases of SJS. People with systemic lupus erythematosus or HIV infections are more susceptible to drug-induced SJS.

Infections

Ø In pediatric cases, Epstein-Barr virus and enteroviruses have been associated with SJS.

Ø Recent upper respiratory tract infections have been reported by more than half of patients with SJS.

Ø Bacterial infections linked to SJS include group A beta-hemolytic streptococci, diphtheria, brucellosis, lymphogranuloma venereum, mycobacteria, Mycoplasma pneumoniae, rickettsial infections, tularemia, and typhoid.

Ø Fungal infections with coccidioidomycosis, dermatophytosis, and histoplasmosis are also considered possible causes. Malaria and trichomoniasis, protozoal infections, have also been reported as causes.

Sinusitis

v Sinusitis is an inflammation or swelling of the tissue lining the sinuses. Healthy sinuses are filled with air. But when they become blocked and filled with fluid, germs can grow and cause an infection.

v Conditions that can cause sinus blockage include:

a.  The common cold

b.  Allergic rhinitis, which is swelling of the lining of the nose

c.   Small growths in the lining of the nose called nasal polyps

d.  A deviated septum, which is a shift in the nasal cavity

Types

•     Acute sinusitis usually starts with cold like symptoms such as a runny, stuffy nose and facial pain. It may start suddenly and last 2-4 weeks.

•     Sub acute sinus inflammation usually lasts 4 to 12 weeks.

•     Chronic inflammation symptoms last 12 weeks or longer.

•     Recurrent sinusitis happens several times a year.

•     Immune system deficiencies or medications that suppress the immune system

v For children, things that can cause sinusitis include:

•     Allergies

•     Illnesses from other kids at day care or school

•     Pacifiers

•     Bottle drinking while lying on the back

•     Smoke in the environment

The main things that make sinusitis more likely for adults are infections and smoking.

Acute Sinusitis Symptoms

The main signs include:

•     Facial pain or pressure

•     "Stuffed-up" nose

•     Runny nose

•     Loss of smell

•     Cough or congestion

You may also have:

•     Fever

•     Bad breath

•     Fatigue

•     Dental pain

It may be acute sinusitis if you have two or more symptoms, or thick, green, or yellow nasal discharge.

Chronic Sinusitis Symptoms

You may have these symptoms for 12 weeks or more:

•     A feeling of congestion or fullness in your face

•     A nasal obstruction or nasal blockage

•     Pus in the nasal cavity

•     Fever

•     Runny nose or discoloured postnasal drainage

You may also have headaches, bad breath, and tooth pain. You may feel tired a lot.

All these types of sinusitis have similar symptoms, and are thus often difficult to distinguish. Acute sinusitis is very common. Roughly ninety percent of adults have had sinusitis at some point in their life

By location

There are several paired paranasal sinuses, including the

 1-frontal,

2- ethmoidal,

3-maxillary and

4-sphenoidal sinuses. The ethmoidal sinuses are further subdivided into anterior and posterior ethmoid sinuses, the division of which is defined as the basal lamella of the middle turbinate. In addition to the severity of disease, discussed below, sinusitis can be classified by the sinus cavity which it affects:

•     Maxillary – can cause pain or pressure in the maxillary area (e.g., toothache, or headache)

•     Frontal – can cause pain or pressure in the frontal sinus cavity (located above eyes), headache, particularly in the forehead

•     Ethmoidal – can cause pain or pressure pain between/behind the eyes, the sides of the upper part of the nose (the medial canthi), and headaches 

•     Sphenoidal – can cause pain or pressure behind the eyes, but often refers to the skull vertex (top of the head), over the mastoid processes, or the back of the head

Causes

Maxillary sinusitis may also be of dental origin ("odontogenic sinusitis"), and constitutes a significant percentage (about 20% of all cases of maxillary sinusitis),given the close proximity of the teeth and the sinus floor. The cause of this situation is usually a periapical or periodontal infection of a maxillary posterior tooth, where the inflammatory exudate has eroded through the bone superiorly to drain into the maxillary sinus. Once an odontogenic infection involves the maxillary sinus, it is possible that it may then spread to the orbit or to the ethmoid sinus. Complementary tests based on conventional radiology techniques and modern technology may be indicated, based on the clinical context.

Chronic sinusitis can also be caused indirectly through a common but slight abnormality within the auditory or eustachian tube, which is connected to the sinus cavities and the throat. This tube is usually almost level with the eye sockets but when this sometimes hereditary abnormality is present, it is below this level and sometimes level with the vestibule or nasal entrance.

Treatment

1-Recommended treatments for most cases of sinusitis include rest and drinking enough water to thin the mucus. Antibiotics are not recommended for most cases.

2-Breathing low-temperature steam such as from a hot shower or gargling can relieve symptoms. There is tentative evidence for nasal irrigation. Decongestant nasal sprays containing oxymetazoline may provide relief, but these medications should not be used for more than the recommended period. Longer use may cause rebound sinusitis. It is unclear if nasal irrigation, antihistamines, or decongestants work in children with acute sinusitis

Ayurvedic treatment

1-shnehna

2-shwedna

3-nashya

4-dhumpaan

5-sitopaladi churna 

6-tankan 

7-chandrakant rash 

8-gojihadi kwatha

Leukemia, Lymphoma and Myeloma

Leukemia
Leukemia is cancer of the blood cells, usually affecting the white blood cells, which causes these cells to not work properly. There are four main types of leukemia.
Leukemia can occur in either the lymphoid or myeloid white blood cells.
1- Cancer that develops in the lymphoid cells is called leukemia lymphocytic
2-Cancer that develops in the myeloid cells is called myelogenous leukemia
3-Acute leukemia involves new or immature cells, called blasts, which remain very immature and cannot perform their functions. The blasts increase in number rapidly, and the disease progresses quickly.
4-In chronic leukemia, there are some blasts present, but they are more mature and can perform some of their functions. The cells grow more slowly so the disease progresses gradually

Based on these findings, leukemia is then classified into one of the four main types of leukemias—1-Acute myelogenous leukemia (AML),
2-Chronic myelogenous leukemia (CML),
3-Acute lymphocytic leukemia (ALL), 
4-Chronic lymphocytic leukemia (CLL). In addition to these, there are other types and subtypes of leukemia


Lymphoma
Lymphoma is a type of cancer that originates in the lymphatic system. There are two main types of lymphoma.
1-Hodgkin’s lymphoma, or Hodgkin’s disease, causes the cells in the lymphatic system to abnormally reproduce, eventually making the body less able to fight infection.
2-All other types of lymphoma are called non-Hodgkin’s lymphomas. Cancers that spread to lymph nodes from other parts of the body are not lymphomas.
The lymphatic system, the tissues and organs that produce, store, and carry white blood cells that fight infections and other diseases, includes the bone marrow, spleen, thymus, lymph nodes, and lymphatic vessels. It is important for filtering germs and cancer cells from various parts of the body.
 Lymphoid tissue is found in many places throughout the body, including lymph nodes, the thymus (found behind the chest bone and in front of the heart), the spleen , the tonsils and adenoids, in the bone marrow, and scattered within other systems such as the digestive and respiratory systems.
Risk Factors
• Age—Hodgkin’s disease occurs most often in people between ages 15 and 34, and in people over the age of 55
• Gender—Lymphoma is more common in men than in women
• Family history of lymphoma, particularly brothers and sisters
• Epstein-Barr virus may increase a person’s risk of Hodgkin’s disease
• Acquired immune deficiency syndrome (AIDS)
Risk factors for non-Hodgkin’s lymphoma include:
• Genetic disease of the immune system
• Unprotected exposure to strong sunlight
• A high-fat, low-fiber diet
• Smoking or the use of tobacco products
• Excessive alcohol consumption
• Environmental factors such as radiation, chemicals, and infections
• Organ transplantation
• Infections with human immunodeficiency virus (HIV) or human T-cell leukemia/lymphoma virus (HTLV-1)
• Infections with malaria
• A history of infectious mononucleosis (caused by an infection with the Epstein-Barr virus)
• Helicobacter pylori (H. pylori) bacterium, which has been identified as a cause of stomach ulcers

Myeloma
Multiple myeloma is a type of cancer that affects certain white blood cells called plasma cells. Plasma cells are part of the immune system, which helps protect the body from infection and disease. Like all white blood cells, plasma cells begin their development in the bone marrow, the soft, spongy tissue that fills the center of most bones.
When cancer involves plasma cells, the body keeps producing more and more of these cells. The unneeded plasma cells—all abnormal and exactly alike—are called myeloma cells. Myeloma cells tend to collect in the bone marrow and in the hard, outer part of the bones. In most cases, the myeloma cells collect in various bones, often forming many tumors. When this happens, the disease is called multiple myeloma.
Risk Factors
• Age—Most myeloma patients are between 50 and 70 years old
• Race—The disease affects blacks more often than whites
• Gender—Men are more likely to develop myeloma than women
• A family history of myeloma
• Exposure to certain workplace chemicals and large amounts of radiation
In most cases, people who develop multiple myeloma have no clear risk factors. Scientists believe the disease may be the result of several factors (known and/or unknown) acting together.

Sharir Rachana of guda

In ancient ayurvedic text only single terminology is used to denote the anorectum i.e. Guda it is the organ which actually perform‟s the act of defecation.They have even described the embryological derivation and development of Guda, and other body organs in Sharirasthana. It shows their ingenuity and depth of study of the human body and its organs in those days when facilities were lacking and Sushruta practicing surgery of performing body dissection was considered outcasts and unsociable.

SYNONYMS :

• Apanah

• Braddhanah

• Mahat Srota

• Payu

• Vit Marga

        Guda is the distal part of large intestine having a length of five and half angula (finger‟s); in which there are three vali‟s (folds) namely „Pravahini‟, „Visarjani‟ and „Samvarni‟ proximally to distally. They have the appearance of involuted indentures of counch shell,situated one above the other and coloured like the palate of an Elephant. The total length of vali is four fingers in which each vali having a length of one finger which is separated from each other by a length of half finger. Distal to the lowermost vali i.e. „samvarni‟ at a length of one finger there is presence of „Gudostha‟ having length of one and half Yava i.e. half finger therefore the total length of Guda including „Gudaostha‟ is about five and half angula (finger‟s)

गुदशरीर :-

तत्र स्थुलान्त्रप्रतिबध्दमर्द्धपञ्चांगुलं गुदमाहु ।

तस्मिन् बलयस्तिस्त्रोऽध्यर्ध्दाङ्गुलान्तरसम्भूताः प्रवाहणी

विसर्जनि सव्ंरणी चेति ।

चातुराङ्गुलायताः सर्वस्तिर्यगेकाङ्गुलोच्छ्रिताः ।

शङ्खावर्तनिभाश्चापि उपर्युपरि संस्थिताः ॥

गजतालुनिभाश्चापि वर्णतः सम्प्रकिर्तिताः ।

रोमेन्तेभ्यो यवध्यर्ध्दो गुदौष्ठः परिकिर्तितः ।

                                         -सु  नि २/५

Formation of Guda =

आत्र,गुद,बस्ति उत्पत्ति :-

असृजः श्लेश्मणश्चापि यः प्रसदः परो मतः ।

तं पच्यमानं पित्तेन वायुश्चाप्यनुधावति ॥

ततोऽस्यान्त्राणि जायन्ते गुदं बस्तिश्च देहिनः ॥

                                       -सु शा ४/२६

It is formed by the Prasad bhaga of blood and Kapha, after being digested by Pitta with the help of Vayu.

PESHIES:-

Guda has three Peshies out of sixty six present in kostha.

पेशी वर्णन् :-

पञ्च पेशीशतानि भवन्ति । तासां चत्वारि शतानि शाखासु कोष्ठे षट्षष्टिः ग्रीवां प्रत्यूर्ध्व चतुस्त्रिंशत् ॥

                                       -सु शा ५/४४

DHAMANIES:-

There are twenty four Dhamnies in the body ,out of which ten go downwards and perform the functions of micturation, Defaecation, Ejaculation of Semen, Menstruation and expulsion of foetus during delivery.

SHEERA’S:-

Out of seven hundred sheera‟s present in body there are thirty four Vaata carrying sheera‟s in Kostha; of which eight are present in Guda, Medhra and Shrooni.

Same number‟s of Kapha, Pitta and Rakta carrying sheera‟s are present, hence total of thirty four sheera‟s are present in Guda, Medhra and shrooni region.”

सिरा :-

तासां तु नाभिप्रभवाणां धमनीनामुर्ध्वगा दश,

दशचाधोगामिन्यः चतस्त्रस्तिर्यग्गाः ॥

                                       -सु शा ९/४

GUDA AS MARMA:-

·         Sushruta has described Guda as Sadhyaapraanhar Marma.

गुद मर्म :-

श्रूङ्गाट्कान्यधिपतिः शङ्खौ कण्ठसिरा गुदम् ।

ह्रुदयं बस्तिनाभौ च घ्नन्ति सद्योहतानि तु ॥

                                        -सु शा६/९

सद्योमर्म :-

तत्रवात-वर्चोनिरसनंस्थूलान्त्रप्रतिबध्दंगुदंनाममर्म,तत्रसद्योमरणम्।

                                         -सु शा ६/२६

Charak described Guda as Marma as well as Pranayatan i.e. where   the Prana (life) is situated.Guda is of Mamsa Marma type.

दशप्राणायतनानि

दशप्राणायतनानि,तद्यथा मूर्धा,कण्ठ,हृदयं,नाभि,गुदं,बस्ति,ओजःशुक्रः,शोणितं,

मांसमिति । तेषु षट् पुर्वाणि मर्मसंख्यातानि ॥

                                        -च शा ७/९

गुद मांसमर्म :-

मांसमर्म गुदान्येषां स्नाञ्नि कक्षधरौ तथा ।

                                        -अ हृ शा ४/४५

ASTHI :-

The visceral organs are well protected by the bony age of Shroni. This Shroni comprises of five bones out of them four comes are well attached with Guda, Yoni and Nitamba.and the remaining one is in the Trika region. The Asthi Sandhi of this region is Samudge type.

SNAYU :-

There are sixty snayus in the Pelvic region and eighty are in the Groin. The snayus which are connected with Guda region come under the group of Sushira.Defaecation is the most important function of Guda

STROTAS VICHAR:-

Guda comes under the Bahirmukha Srotos.Guda is mention as to be root of Purish vahaa strotas i.e. faeces carrying strotas.

पुरिष् वह स्त्रो मूलस्थान :-

........पूरिषवहे द्वे तयोर्मूलं पक्वाशयो गुदं च........।

                                         - सु शा ९/१२

SHARIR KRIYA OF GUDA:

Important function of Guda is the excretion of vayu (flatus) and varchas (faecal material); the function is controlled by „Apaan Vayu‟ with the help of three vali‟s. The role of these three vali‟s is of prime importance in this context

शा. क्रिया :-

....मलास्यध्ः पीडनात प्रथमा प्रवाहिणि,गुदविस्फारणेन मलविसर्जनाद् द्वितिया विसर्जनी.गुदसङ्कोचन्याख्यपेशीद्वयकृता चक्राकारा वलिस्त्युसवंरणी नाम् ।

                                       -सु शा २/६,७,८

1) Pravahini vali:-

As the name suggests it help‟s to propel or force the faecal material downwards.

2) Visarjani vali:-

Relaxes the anorectal muscle and thus performs excretion of faeces.

3) Samvarni vali:-

It closes the anal orifice after the faecal material is expelled by the action of Visarjani.

According to Acharya Charaka, Guda is one of the fifteen organs belonging to Kostha. Further, he has divided it into two parts viz., Uttar Guda and Adhar Guda. It is difficult to make a line of demarcation between the Uttar Guda and Adhar Guda. Here the commentator Chakrapani comments that Uttar Guda is a part of Guda which stores the faeces and the Adhar Guda is the lower part of Guda which is related to defaecation.

Guda-ashrit vyadhi.

1)Arsha     2)Parikartika  3) Bhagandara  4)vidradhi

Ø  Arsha

As described in Sushrut Samhita “Arsha‟ covers a vast topic. While describing the treatment of  “Guda-arsha‟ acharya Sushruta have mentioned four modalities of treatment viz.

1) Bhesajam i.e. treatment by medicines

2) Kshara pratisaran i.e. local application of kshara(alkali of herbal drug)

3) Agani karma i.e. cauterisation

4) Shastra karma i.e. surgical treatment.

Classification of Arśa

There are different opinions of Aacharyas  regarding the classification of Arsha. They are classified on the basis of origin, bleeding and predominance of Doshas etc. This classification is as follows:-

The classification on the basis of the origin

1. Sahaja

2. Janmottarakālaja

Sahaja Arsha is considered to be congenital anomaly due to disorders of paternal and maternal chromosomes. It is very difficult to diagnose because of its different size and shape. Janmottarakālaja Arsha occurs due to the malpractices in daily life like faulty food habits and regimen .

The classification on the basis of the bleeding nature

Aacharya Charaka has stated these two types of Arsha while describing the Chikitsa. He stated it as Ardra and Sushka .Ardra also called as Starvi, are bleeding piles due to vitiation of Asruka and Pitta mainly. Aacharya Vagbhatta has again divided it into Vatanubandhi, Pittanubandhi and Kaphanubandhi. While other Sushka Arsha are non bleeding pile masses due to vitiation of Vata and Kapha.

The classification on the basis of the predominance of Doşa

It is mainly sub division of the Janmottarkālaja type of Arsha. According toAacharya Charaka and Vagbhatta, it is of five types while Aacharya Sushrutadifferentiates it into four types.He omitted the Dwandaja variety. Sixtype of Arsha are mentioned similar to Charaka in Yoga Ratnakara, MadhavaNidan, Harita Samhita and Bangasen Samhita

The classification on the basis of prognosis

1. Sadhya (Curable),

2. Yapya (Palliative)

3. Asadhya (Incurable).

• Sadhya variety: According to Aacharya  Sushruta if the Arsha is located in the Samvaraņi and is of single Doshika involvement and not very chronic and it will be curable (Sadhya).

• Yapya variety: The Arsha caused by the simultaneous vitiation of any two Doshas and the location of Arsha in the second Vali, the chronicity of the disease is not more than one year, it can be considered as Yapya variety.

• Asadhya variety: Sahaja Arsha, if caused by the vitiation of three Doshas and if the Arsha is placed in the internal Vali, is incurable. In addition to this if the patients develops edema in hands, legs, face, umbilical region, anal region, testicles and if he suffers from pain in the cardiac region, it is considered as incurable. Aacharya Charaka stated that Arsha located in Samvarņi Vali with involvement of only one Dosha and less chronic are treated as Sadhya. The Arsha located on second Vali i.e. Visarjaņi with involvement of any two Doshas and the chronicity is not more than one year are treated as Yapya. While Sahaja Arsha, situated at third Vali i.e. Pravahiņi and having involvement of three Doshas and chronicity more than one year are treated as Asadhya.

The classification on the basis of management

On the basis of the treatment, Arsha can be classified into four varieties as follows.

•       Bhaishaja sadhya Arsha.

•       Kshara sadhya Arsha

•       Agnikarma sadhya Arsha

•       Shastra sadhya Arsha

Ø  Parikartika

In Ayurvedic literature a number of conditions have been described in relation to ano-rectal region or Guda. But such a picture is not completely found in any one of them. It is surprising to note that although it is one of the common ailment in ano-rectal area, still it escaped the notice of the ancient scientists. However, a detailed exploration of literature suggests some words which clinically may resemble these particular entity. It may be worth wile to mention here that the Ayurvedic practitioners have recently coined a word ‘ Gud-Vidar’ to represent this condition, but this word does not have any origin in the original classics of Ayurveda.        

Description of this condition is very much suggestive of the modern ailment fissure-in-ano when it is limited to anal-region. Ancient literature including Vedas have a rich description of various diseases and their management. But “Parikartika” is not described in Vedas, and other authors have paid very poor attention to its description as compared to other diseases. This may be attributed to excellent general conditions, of health, hygiene and natural habitat of ancient people.

The prodromal symptom in the words of Sushruta is pain of sharp cutting nature in the Guda. Further he has described in chapter Vaman Virechan Vypada, there is sort of cutting pain, sawing pain in the anus, penis, umbilical region and the neck of the urinary bladder.

Ø  Bhagandara =

Bhagandara derives its name from two words 'Bhaga' and 'Darana'.

Bhaga : The term Bhaga has been used for different entities by different authors.

Darana : means splitting or discontinuity with severe pain .

Thus, Bhagandara is a disease which causes splitting or discontinuity in the region of Bhaga, Basti and Guda region.

Charaka and Vagbhata have given detailed description of general etiology of Bhagandara. (Ch.chi. 14/ Va.Ni  8 )

Sushruta also given the etiology of Bhagandara. (Su.Ni.4)

Vata-pitta-kapha, prakopaka ahara & vihara,Hard stool (vegavrodha) etc.

Types =

According to sushruta

                             Vataja -             shataponak

                            Pittaja-                ushtagreeva

                            Kaphaja-              paristravi

                             Sannipataja -       shambukavarta

    Aagantuja-          unamargi

According to vagbhat 

                             Vatapittaja-       parikshepi

                             Vatakaphaja-        ruju

    Kaphapittaja-        arshobhagandra.

Aacharya Sushruta explains Abhyantara vidradhi out of which Gudagat can correlate with Ano-rectal abscesses.

Modern Review of literature.

To understand the aetiopathogenesis of various Ano-Rectal diseases it is wise to know the anatomy of the concerned region.

Derivation Of Rectum And Anal Canal:

1. Rectum :

 The rectum is derived from the primitive rectum i.e. the dorsal subdivision of the cloaca. According to some authorities the upper part of the rectum is derived from the hind gut proximal to the cloaca.

2. Anal Canal :

The anal canal is formed partly from the endoderm of the primitive rectum and partly from the ectoderm of the anal pit or proctodaeum. The line of junction of the endodermal and ectodermal part are represented by the anal valves.

Ø  The anatomical anal canal extends from the anal valves to the analverge.

Ø  The surgical anal canal commences at the level where the rectumpasses through the pelvic diaphragm and ends at the anal verge.

ANAL CANAL MUSCULATURE:

The internal sphincter is a thickened continuation of the circular muscle coat of the rectum. This involuntary muscle commences where the rectum passes through the pelvic diaphragm, and ends just within the anal orifice, where its lower border can be felt. The internal anal sphincter is 2.5 cm. long and 2 to 4 mm thick when exposed during life, it is pearly - white in colour and its individual transversely placed fibres can be seen clearly. Spasm and contracture of this muscle play a major part in fissure and several other anal affections. The conjoined longitudinal muscle is a continuation of the longitudinal muscle coat of the rectum intermingled with fibres from the pubo-rectalis. Some of its fibres pass through the Anal internal sphincter to reach the submucous space, and are inserted into the fibrous tissue beneath the anoderm, but they mainly fan out through the lowest part of the external sphincter, to be inserted into the true Anal and perianal skin, thus constituting the corrugator cutis ani of Ellis. Other fibres pass more laterally across the Ischio rectal, fossa, while anteriorly fibres of this muscle are inserted into the triangular ligament, the urethra and the apex of the prostate, thus constituting the recto-urethralis muscle. The external sphincter, formerly subdivided into a deep, superficial and subcutaneous portion is now considered to be one muscle. Some of its fibres are attached posteriorly to the coccyx, while anteriorly they are inserted into the mid-perineal point in the male, where as in the female they fuse with the sphincter vagina. In life the external sphincter is pink in colour, and homogenous.

The conjoined longitudinal muscles, by traversing the internal and external sphincters to reach their insertions, serve to brace these sphincters.

THE MUCOUS MEMBRANE:

The pink columnar epithelium lining the rectum extends through the ano-rectal ring into the surgical anal canal. The mucosa of the surgical Anal canal is attached loosely to the underlying structures, and covers the internal haemorrhoidal plexus. Passing downwards where it clothes the series of 8 to 12 longitudinal folds known as the columns of Morgagni, the mucous membrane becomes cubical and red in colour; above the anal valves the mucous membrane becomes plum coloured. Just below the level of the Anal valves there is an abrupt, albeit wavy, transition to squamous epithelium, which is parchment colour. This wavy junction constitutes the dentate line. The squamous epithelium lining the anatomical Anal canal is thin and shiny, and is known as the Anoderm. The Anoderm passes imperceptibly into the pigmented skin of the anus. Below the dentate line the anoderm is attached very firmly indeed to deeper structures.

THE DENTATE LINE

is most important landmark both morphologically and surgically. It represents

1. The site of fusion of the proctodaeum and post allantoic gut and

2. The position of the Anal membrane, remnants of which may frequentlybe seen as Anal papillae situated on the free margin of the Anal valves.

 Anatomical and Surgical importance of the Dentate line:-

1) It forms the embryological watershed between visceral structure above and somatic structure below.

2) The mucosa above the line has autonomic nerve supply and is thus insensitive to cutting and pricking where as the skin and mucosa below is supplied by the inferior rectal branch of the pudendal nerve and is actually sensitive to these stimulii.

3) The anal glands open into the anal sinuses above the anal valve at this level. Infection in an anal gland may lead to an anal abscess which may extend into ischiorectal space and perianal space .

4) In the finer control of continence stimulation of nerve endings in the region of the dentate line may initiate reflex or voluantry changes on sphincter tone.

 The Dentate line seperates:-

Above                                                                      Below

Cubical epithelium                                       Squamous epithelium

Autonomic nerve                                         Spinal nerve

(Pain insensitive)          (Very much pain sensitive)

i.e. Pudendal nerve

Portal venous system                                   Systemic venous system

THE ANAL VALVES OF BALL are a series of transversely placed semilunar folds linking the columns of a Morgagni. They are functionless remnants of the fusion of the post allantoic gut with the proctodaeum.

THE CRYPTS OF MORGAGNI [ANAL CRYPTS] are small pockets between the inferior extremities of the columns of Morgagni. Into several of these crypts, mostly those situated posteriorly, opens one Anal gland by a narrow duct. This duct bifurcates, and the branches pass outward to enter the internal sphincter muscle, where often there is situated an ampulla issuing from this ampulla there are three to six tubular sub-branches that extends into the inter muscular connective tissue, where they end blindly. As a rule it is the caudal branch that is furnished with sub-branches, where as the cephalad branch remains a solitary simple tubule and therefore, when infected, is more likely to discharge its purulent contents along the lumen of the duct than to form an abscess. In some lower animals these glands secrete an odoriferous substance during the rutting season; in man their function. If any, is obscure.

Some of their cells have been shown to give a positive staining reaction for mucin, but as the lining epithelium is mainly cubical, the mucous secreting proper of the Anal glands must be extremely small infection of an Anal gland is the most common cause of ano-rectal abscesses and fistulae.

The Rectum:

The rectum extends from the third sacral vertebra to the ano-rectal ring. It describes three lateral curves, two concave to the left [hence the left lateral position for sigmoidoscopy and one concave to the right. The relative shortness of the longitudinal muscle coat forms the valve of Houston that are so much in evidence in sigmoidoscopy. Layers of the Rectum:-

As part of large intestine it has all the four layers in wall

1) The mucosal

2) The submucosal

3) The circular muscle

4) The longitudinal muscle

The Ano - Rectal Ring:

The Ano-rectal ring marks the junction between the rectum and the anal canal. It is formed by the fusion of the pubo rectalis muscle, external sphincter, conjoined longitudinal muscle, and internal sphincter. The Ano-rectal ring can be clearly felt digitally, especially on its posterior and lateral aspects. Division of the Ano-rectal ring results in permanent incontinence of faeces.

Fascia of the rectum:

LATERAL LIGAMENTS: Condensations of areolar tissue around the middle rectal vessels from the lateral ligaments of the rectum. These ligaments have to be divided during excision of the rectum.

FASCIA OF WALDEYER: the rectum can be lifted forward by blunt dissection from the concavity of the sacrum and coccyx. When this has been done, one finds a strong thick layer of parietal pelvic fascia adherent to the sacrum and coccyx, known as the fascia of Waldeyer. Traced inferiorly on the upper layer of the anococcygeal ligament, the fascia fuses with the rectum at the ano rectal junction. The fascia of Waldeyer is clearly seen as a thick white layer of fascia after the anococcygeal ligament has been divided during perineal excision of the rectum. The fascia has to be divided to gain success to the retrorectal space. If the surgeon fails to incise this ligament he will dissect posterior to it, in which case serious haemorrhage will occur due to injury to the sacral veins.

FASCIA OF DENONVILLIERS: Anteriorly the extra peritoneal rectum is covered with a closely adherent layer of visceral pelvic fascia, which extend from the anterior peritoneal reflection above to the superior layer of the urogenital diaphragm below and laterally becomes continuous with the lateral ligaments of the rectum. This fascia is the fascia of Denonvilliers. During excision of the rectum for cancer, this fascia together with the rectum is separated from the anteriorly placed seminal vesicles in the male and the vagina in the female. At the level of the base of the prostate, the fascia of Denonvilliers is incised transversely to develop a plane of dissection between it and the rectum. The fascia of Denonvilliers remains adherent to the posterior aspect of the prostate gland.

SUPPORTS OF THE RECTUM:

The end gut is held in position by:

1.The attachments of the levatores ani between the internal and

sphincters.

    2. The visceral layer of the pelvic fascia.

    3. The recto-urethralis muscle, which attaches it to the urogenital

diaphragm and perineal body.

    4. The rectal stalk or lateral ligament. On each side of the back of therectum, 2 – 5 cm above the levator, is a dense fibrous cord runningfrom the third piece of the sacrum to the rectal wall. It contains the nervi erigentes (S2, S 3) and the middle rectal arteries, and is an important structure in holding up the rectum. The surgeon cannot draw down the rectum in the operation of perineal excision till this ‘stalk’ is divided.

5. The fatty tissue of the pelvis and ischiorectal fossae.

6. The sacral curve, which is not well marked in the infant and child.

The Blood Supply:

1. The Superior Haemorrhoidal Artery :

This artery is the direct continuation of the inferior mesenteric artery and constitutes the chief arterial supply to the rectum. Opposite the third sacral vertebra the artery divides into a right and left branch, which descend on the postero - lateral walls. About halfway down the rectum each branch subdivides and pierces the rectal wall. The terminal branches run straight downwards each in a column of Morgagni.

The Middle Haemorrhoidal Artery:

This artery is usually so small as to be almost insignificant arises on each side from the internal iliac artery and supplies the muscle coat of the mid-rectum. These arteries anastomose freely with the superior and inferior haemorrhoidal arteries.

The Inferior Haemorrhoidal Artery:

This artery is arises on each side as a branch of the internal pudendal artery, as this artery enters Alcock’s canal crossing the upper part of the Ischio rectal fossa, it breaks up into branches which supply the anal sphincters, anal canal and the skin of the anal margin.

The Internal Haemorrhoidal Venous Plexus:

This lies in the loose submucosa of the anal canal and extends from the level of the dentate line to that of the ano-rectal ring. The plexus drains into about six collecting veins, which are situated in the submucosa of the rectum. About half way up the rectum these branches pass through the rectal wall, and having reached the out side of the rectum, they unite to form the superior haemorrhoidal vein, an important tributary, of the portal vein. The middle haemorrhoidal veins are small and drain into the internal iliac veins.

The external haemorrhoidal venous plexus:

This lies under the skin of the anal canal below the dentate line and beneath the skin of the anal margin. Communicating veins pass from the external haemorrhoidal plexus to the internal haemorrhoidal plexus beneath the anoderm. The lower part of the external haemorrhoidal plexus drains into the internal pudendal veins and then into the internal iliac veins, thus providing a link between the portal and systemic venous system.

The Lymphatics of the Ano-Rectum:

The collecting lymphatic vessels of the surgical anal canal are divided into two networks. One beneath the mucocutaneous lining and the other related to the muscular coats. Although these are distinct systems, it becomes apparent that there is plentiful inter communication between them, particularly along the points of penetration of the muscular walls of the anal canal by blood vessels. From these networks emerge three sets of lymphatic trunks referable to the lower, middle and upper thirds of the anal canal.

The lymphatics of the rectum proper:

The lymphatic plexuses of the rectum proper are divided into an intramural and an extra mural group. The intramural system is redivided into two fairly distinct territories at the level of the middle valve of Houston. The lower part of the plexus drains downwards to join the lymphatic trunks that follows the middle haemorrhoidal vessels; the upper trunks follows the superior haemorrhoidal vessels to the lymph nodes in the meso rectum and meso-colon. The extra mural plexus drains into a group of 4 to 7 lymph nodes situated above the levator ani, in the region of the ampulla, in close relation to the rectal wall. These are the para rectal lymph nodes of gerota. Larger lymph nodes are situated more superiorly at the level of the third piece of the sacrum, opposite, which the superior haemorrhoidal artery bifurcates.

Proceeding upwards, the lymphatic trunks of both plexus pass to nodes situated at the origin of superior haemorrhoidal artery and the sigmoidal arteries. From there the lymphatic trunks pass to the upper most nodes grouped around the origin of the inferior mesenteric artery. There is seldom, if ever, metastasis along the lateral or inferior lymphatic pathways from a carcinoma situated above the ampulla of the rectum. Hence, in general it can be stated that the higher the growth the more confined are its metastasis. This justifies restorative resection in cases of carcinoma high in the rectum.

Nerve supply:

Above the dentate line the rectum and anal canal is supplied by sympathetic and parasympathetic nerve fibres. The sympathetic supply is comprised by branches of inferior mesenteric plexus and presacral nerves from preaortic plexus commencing in the 2nd, 3rd and 4th lumber sympathetic ganglia, while the parasympathetic supply comes from the 2nd, 3rd and 4^th sacral nerves. The main function of the sympathetic nerve is to inhibit the rectal wall and stimulate the internal sphincter, where as, the parasympathetic nerves stimulate the rectal wall and inhibit the sphincter. Afferent impulses underlying sensations of physiological distension are conveyed by the parasympathetic nerves, while pain impulses are conducted by both the sympathetic and parasympathetic nerves. The inferior haemorrhoidal nerve supply the distal portion of pectinate line and part of the external sphincter. The external sphincter - ani is also supplied by the perineal branch of the fourth sacral nerve.

Function:-

1) To increase peristaltic movement and sensory activity.

2) To open or relax internal sphincter.

Physiology Of Defecation:

Defecation is an act of emptying of entire distal colon from the splenic flexure through the anal orifice into the exterior, which is a reflex process. The reflex is initiated by the rise of intra luminal pressure of about 20-25 cm of water in the rectum containing pressure receptor, which not only detects increase of pressure but also differentiates whether the increase in pressure is due to gas, liquid or solid. The reflex centres have been located in the hypothalamus, in the lower lumber and upper sacral segments of the spinal cord and in the ganglionic plexus of the gut. This is a reflex which is under some degree of voluntary control.

Mechanism:

The rectum is normally empty. The faecal matter is stored in the sigmoid and pelvic colon and not in the rectum. As soon as some faecal matter enters the rectum due to mass movement there is a desire for defecation along with voluntary effort e.g. assumption of appropriate posture, voluntary relaxation of external anal sphincter and abdominal compression in the adult, etc. which may further augment visceral reflexes. These reflexes result mass contraction of entire length of colon and relaxation of internal anal sphincter. Thus the colon contents pass into the pelvic colon, rectum, anal canal and finally removed from the body. Defecation reflex can be initiated earlier or inhibited voluntarily.

 Various Ano-rectal diseases

1) Haemorrhoids2)Anal fissure3)Anal fistulas      4)Abscess

Ø  HAEMORRHOIDS OR PILES

Dilated tortuous veins i.e. varicosity of the vein of anal canal is known as haemorrhoids.

Haemorrhoids or Piles is one of the commonest ailments affecting mankind due to evolution i.e. erect posture.

CLASSIFICATION

I) Internal haemorrhoid:-

Arising in upper 2/3rd of the anal canal which is lined by columnar epithelium above dentate line.

II) External haemorrhoid:-

Arising in skin in lower anal canal below the dentate line.

DEGREE OF HAEMORRHOID FORMATION

There are four degrees of internal haemorrhoids

I) First degree haemorrhoid ( Io )

These merely projects slightly into the lumenof anal canal when the veins are congested at defecation.

II) Second degree haemorrhoid ( IIo )

These piles tend to form swelling which not only protrude into the anal canal but also descend towards the anal orifice so that eventually the mucosal surface corresponding to the pile may appear externally while the patient is straining, but return spontaneously to the anal canal when motion has passed and defecation efforts has ceased.

III) Third degree haemorrhoid ( IIIo )

These piles prolapsed more readily and not only protrude during defecation but remain prolapsed afterward until they are digitally replaced in the anus.

IV) Fourth degree haemorrhoids ( IVo )

These piles are very large and develop considerable skin covered component that they cannot be properlyreturned to the anal canal but instead remain as a permanent projection of the anal mucosa

Ø  Anal Fissure =

Anal fissures are common problems that cause severe patient discomfort. A fissure is basically a linear tear in the anal mucosa which extends distally from the dentate line to the anal verge. Analogous to a “split lip” of the anus, every time a patient has a bowel movement, the anal mucosa will be stretched and the fissure reopened. A fissure can sometimes heal by itself, but due to recurrent injury by the mechanism described above, and often the associated increased contraction of the internal anal sphincter, it becomes a chronic problem.

Etiology/Epidemiology =

The etiology for anal fissures is not completely understood. Some type of initial trauma is necessary with subsequent failure of healing. This initial insult is often a hard bowel movement and history of constipation, although severe diarrhea can also be an associated condition as well. Other diseases like Crohn’s disease, HIV or previous surgery should also be considered. Failure of healing is thought to be secondary to internal anal sphincter hypertonicity and subsequent relative decreased blood supply.

Diagnosis =

A thorough history is not only essential, but can often make the diagnosis alone in this disease. Patients will describe a sharp pain that is initiated by a bowel movement. The pain will last for a few minutes to several hours. Other complaints will be bright red bleeding after a bowel movement that is most commonly described as streaking the stool or on the toilet paper with wiping, although it can occur throughout the day. If a sentinel pile is present, some tenderness to palpation can be present. On examination spreading of the buttocks is often enough to see the fissure and no anoscopic exam is necessary in the acute setting. Digital rectal examination can often palpate these fissures, although local anesthetics are recommended due to the severe pain associated with such an exam. It is the authors’ preference to diagnose and begin treatment (often without digital examination or anoscopy) and bring the patient back in 2-4 weeks for a more thorough examination when the patient is less symptomatic.

Management =

Again conservative management is the first option in treatment. Medical management includes oral analgesics, sitz baths, bulking agents and/or stool softeners, increased hydration and topical anesthetics.

If the fissure fails to heal after medical treatment, surgical intervention is often necessary. Although many procedures have been reported, the lateral internal sphincterotomy (LIS) is the most commonly performed. This procedure involves division of the internal anal sphincter muscle to the level of the proximal extent of the fissure or the dentate line through either a closed or open procedure.  This relieves the symptoms in over 98% of patients and has very low recurrence rate. Other surgical approaches include posterior internal sphincterotomy and manual anal dilation which are each associated with higher complication rates of a keyhole defect and fecal incontinence.

Ø  Fistula- in- Ano

Ø  Fistula in ano  is a disease of ano rectum which is characterized by single or multiple sinuses with pulurent discharge in perianal region.

Ø  Fistulous track lined by granulation tissue-opens deeply in the anal canal or the rectum and superficially on the skin around the anus.

Etiology =

Nonspecific (90%)

·         Cryptoglandular origin

Specific (10%)

·         Anorectal disease

·         Inflammatory bowel disease

·         Infections

·         Malignancy

·         Trauma

Some other causes

·         Previous pyogenic abscess

·         Tuberculosis

·         Ulcerative colitis

·         Crohn’s disease

·         Other abdominal disease leading to formation of pelvic abscess.

Signs & Symptoms =

·         External opening : A boil in the perianal region with purulent, or serous discharge with skin irritation.

·         Intermittent swelling, pain, and fever.

·         Chronic draining sinus.

·         Sometimes multiple ext. openings- “watering-can” appearance.

·         Internal opening as a fibrous dimple may be seen or felt in digital exam.

Classification =

·         Sub-cutaneous fistula

·         Sub-mucus fistula

·         Inter-sphincteric fistula

·         Trans-sphincteric or Ischiorectal fistula

·         Extra-sphincteric or Pelvirectal fistula

MILLIGAN & MORGAN (1934) & GOLIGHER (1975)

·            SUBCUTANEOUS (5%)

·         LOW ANAL (75%)

·      HIGH ANAL (8%)

·            ANORECTAL(7%)

·            ISCHIORECTAL OR INFRALEVATOR

·            PELVECTAL OR SUPRALEVATOR

·            SUBMUCOUS (OR HIGH INTERMUSCULAR) (5%)

Anorectal Abscess=

An anorectal abscess is essentially a “boil” of the perianal/perirectal region, with the purulent collection developing as the acute manifestation, and the anal fistula resulting as a consequence of this initial infection.

Etiology/Epidemiology =

        The etiology of these abscesses is thought to be cryptoglandular in approximately 80% with the remaining 20% being from trauma, HIV, cancer, or inflammatory bowel disease . These very common infectious processes develop when there is an obstruction of an anal crypt at the dentate line in the anal canal. The anal gland emptying into that crypt then becomes infected and, depending on the exact location of the infection, a perianal or perirectal abscess arises. Such an abscess is either drained surgically or drains spontaneously. If the opening to the anal crypt does not heal completely, this becomes the internal opening of a fistulous tract that drains through the external opening on the anus or buttock where the abscess originally drained.

Diagnosis =

Common presenting symptoms for abscesses include pain, swelling and other general signs of an infection, including fever, especially in ischiorectal and supralevator abscesses. The pain is classically severe in the perianal or perirectal region, and mostly gradual in onset. Pain is not often associated with fistulas, where drainage and occasional bleeding is more common. On examination, a tender fluctuant mass can be seen if a perianal abscess is present.Unfortunately, patients with intersphincteric, supralevator and deep post-anal space abscesses may have a paucity of findings other than tenderness with digital rectal examination.

Management

A simple abscess without a fistula can be incised, drained and the wound left open for continued drainage. An elliptical or cruciate incision is often preferred. Perianal and ischiorectal abscesses can be drained in the OT with the aid of  anesthetics. If the abscess is large, the patient is febrile, or other types of abscesses are suspected (i.e., supralevator, deep postanal space, horseshoe abscess) it is best performed, if possible, in the operating room under general anesthetics.

Ø  Complications

Post-operative complications include recurrence of the abscess or fistula.

Complications of Ano-rectal surgery =

·         Primary haemorrhage

·         Secondary haemorrhage & sepsis

·         Anal stenosis

·         Anal incontinence

Management of haemorrhage =

·         Anal packing

·         Haemostatic agents – adrenaline / Sepgard pack.

·         Cauterization or ligature  under anaesthesia

Anal stenosis =

·         Anoplasty

Anal incontinence =

·         Sphincter exercises 

·       Sphincter repair

·       Graciloplasty / Gluteus maximus repair