Constipation With Susruta Ayurveda

Understanding Constipation with Susruta Ayurveda

by with One Comment Gastrology

What is constipation?

Constipation is a very common gastroenterological disorder experienced by almost one-fifth of the population. Constipation refers to bowel movements that are infrequent or hard to pass and is a common cause of painful defecation.

Characterized by

  • passing hard stool
  • Incomplete emptying of Bowel
  • Straining
  • Reduced frequency of stool 3 times or less than 3 times in a week
  • Manual maneuvers to pass stool

It must include 2 or more 2 characters from the list.

You can assess the level of constipation with the character of the stool as per the Bristal stool chart which is available on the Internet

Causes of Constipation 

  • Stress
  • Lack of intestinal movement
  • Diabetes
  • Less fluid intake
  • Less fiber diet intake
  • Iron or Aluminum supplement
  • Pregnancy
  • Late night awakening

Types – It may be acute or chronic

 

Treatment 

The basic aim of treatment is to find out the cause and treat it.

  1. Dietary adjustment: Fibre supplementation is the first line of therapy for normal or slow transit constipation e.g. Wheat bran, vegetables, fruits, mucilage, corn, and cellulose.
  2. Behavioral therapy: Habit training is important to achieve regular defecation. The patient is advised to attempt defecation after meals when colonic motility is maximum.
  3. Drug Treatment: Include consumption of Laxatives which may be of   Osmotic, Stimulant, Bulk-forming (fiber) type or a softener or maybe Lubricant

But there are some limitations to this treatment as long-term intake may cause some structural changes in the gut mucosa

  • Other adverse effects- interference with co-concomitant drug

How AYURVEDA can help you? 

But to treat constipation is more straightforward with Ayurveda, and how it is achieved let’s find out

Firstly as per Ayurveda principles – Eliminate the cause of constipation by avoiding stress or more liquid intake if these are the causes.

The line of treatment for constipation includes fomentation, massage, tub baths, suppositories, and enema, and having foods and drinks which are laxative.

Rasa’s role in stool evacuation

  • sweet, sour, and saline tastes are useful for the elimination of stool whereas drugs and diets having pungent, bitter, and astringent taste creates difficulty in the elimination of stool.

Virechana is a therapeutic modality to treat constipation which is of majorly 3 types

  • Sukha Virechana/ easy purgation) e.g;  Trivrit  (Operculina turpethum)
  •  Mridu  virechana /mild  purgation) e.g;  Aragvadha  (Cassia fistula)
  • Tikshna Virechana /strong purgation) e.g; Milk of sushi (Achyranthes Aspera)

Some Ayurveda Literature drugs are also having good results like

  • Haritaki (Terminalia chebula)
  • Aragvadha (Cassia fistula)
  • Katuki (Picrorhiza kurroa)
  • Trivrit (Operculina turpethum)
  • Isabgol (Plantago Ovata)

Lastly simpler one which is readily available at your Home- A glass of Luke’s warm Water

To experience good results please consult your Ayurveda Doctor before intake or visit our site to take an appointment

Know About Your Ulcers In Stomach

Buy Gynoveda Constipation Fast Relief Medicine | Ayurvedic Colon Cleanser For Gut health | Natural Laxative Haritaki Castor Oil Improves Digestion |Goodbye Isabgol, Powder, Triphala | 

 

Constipation

Ulcer

Know About Your Ulcers In Stomach

by with One Comment Gastrology

Peptic Ulcer

A peptic ulcer is defined as a disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation. The word peptic refers to pepsin a stomach enzyme that breaks down proteins. A peptic ulcer in the stomach is called a gastric ulcer.

Epidemiology of Peptic ulcer

Peptic ulcers used to be a rare disease before the 19th century. Acute perforations of gastric ulcers were first reported in young girls at the beginning of the 19th century. With the progress of the 19th century, peptic ulcer disease became frequent both in men and women.

In the West, this disease affects equally men and women whereas men are affected 18 times more commonly than women in India.  Broadly, in developing countries like India, it is impossible to obtain exact figures for disease incidence, and differences are bound to exist between regions.

A peptic ulcer is more prevalent in Jammu and Kashmir, followed by Southern India. North India comes next, and East and North East have a comparatively lower prevalence

Pathogenesis of Peptic Ulcer

Peptic ulcers occur because of an imbalance between aggressive factors (gastric acid and pepsin) and defensive factors (gastric mucus, bicarbonate, Prostaglandins). Gastric ulceration occurs when mucosal defenses fail, as when mucosal blood flow drops, gastric emptying is delayed, or epithelial restitution is impaired

The factors produce ulceration by aggravating gastric acid and pepsin secretion- 2 categories:

a. Endogenous factors: These include different visceral neurotransmitters, hormones (acetylcholine, gastrin, histamine, somatostatin, and cholecystokinin), second messengers (Ca2+), and genetic factors.

b. Exogenous factors: These include bacterial infection (H. Pylori), NSAID, alcohol, psychogenic factors, and dietary habits.

Endogenous Factors

  1. Acetylcholine (Ach)
  2. Gastrin
  3. Histamine
  4. Somatostatin and Cholecystokinin:
  5. Ca2+ as second messengers
  6. Genetics: Increased familial history – 20-50% of patients. Ulcers are also more common in blood group O subjects and in those who do not secrete blood group antibodies into gastric secretions.

Exogenous Factors

  1. H. pylori: Pylori is a curved or S-shaped gram-negative bacterium approximately 0.5 by 3 µm in size containing four to seven sheathed flagella at one pole.
  2. Non-steroidal Anti-inflammatory Drugs (NSAID): NSAIDs interferes with the following lines of mucosal defense-
    • Mucous cell secretion of mucin and surface-active phospholipid. Both PGE and PGF induce the secretion of polysaccharide material in the stomach known as mucin, which acts as a protective agent against potential stomach ulceration induced by HCl and pepsin. This implies that NSAIDs cause gastric ulcers by inhibiting the secretion of this cytoprotective substance.
    • Basal bicarbonate secretion from gastric mucosa.
    • Mucosal proliferation is necessary for ulcer healing.
    • Regulation of mucosal blood flow.
    • Physiological regulation of gastric acid secretion via feedback inhibition.

    NSAID may also cause ulceration by the generation of oxygen-derived free radicals and products of the lipo-oxygenase pathway. COX inhibition by NSAID results in the diversion of arachidonic acid metabolism towards the lipo-oxygenase pathway, resulting in increased leukotriene synthesis. These leukotrienes can contribute to gastrointestinal ulceration, through two mechanisms, firstly, by a reduction in prostaglandin level and secondly, through the release of oxygen radicals mediated mucosal injury produced in this pathway.

  3. Ethanol:  Ethanol damage to the gastrointestinal mucosa starts with micro-vascular injury, namely disruption of the vascular endothelium resulting in increased vascular permeability, edema formation, and epithelial lifting. These effects are secondary to ethanol-induced slowing or cessation of gastric mucosal flow. Alcohol causes the stomach cells to oversecrete both acid and histamine which makes the stomach linings vulnerable to ulcer formation. Ethanol also reduces prostaglandin levels and increases the release of histamine and the influx of calcium ions.
  4. Cigarette Smoking: Continued smoking with advancing age augments the secretion of HCl and pepsin and is also expected to modify the contents of gastric juice and pepsin isoenzyme patterns. The increased gastric acid secretion is mediated through the stimulation of the H2-receptor by histamine released after mast cell degranulation and due to the increase of the functional parietal cell volume or secretory capacity in smokers. Smoking causes mucosal injury by increasing the content of free oxygen radicals, PAF, pituitary vasopressin, gastric endothelin, and pituitary vasopressin. Smoking and nicotine stimulate pepsinogen secretion also by increasing the chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H. pylori, alcohol, NSAID or cold restrain stress. Smoking also alters processes important in gastric and duodenal mucosal integrity or protection such as mucosal bicarbonate secretion, prostaglandin content, mucosal blood flow, or epidermal growth factor.
  5. Diet: All foods are capable of stimulating gastric acid secretion through distention of the stomach, but proteins are the major stimulants. Digested proteins in the form of peptides, peptones, and amino acids act primarily through the stimulation of gastrin from antral G cells. The aromatic amino acids are the most potent of the amino acids. Amino acids absorbed into the circulation stimulates acid secretion by directly stimulating parietal cells or via gastrin release in humans. Caffeinated beverages (eg. tea, coffee), cola-type beverages, beer, and milk are potent stimulants of gastric acid secretion. Coffee produces acid output equal to 70 percent of peak acid output as compared to Penta gastrin. 5% aqueous tea and coffee beverages act by decreasing PGI2 synthesis. A low-fiber diet, and high dietary consumption of salt and red/black peppers also cause peptic ulcers.
  6. Psychological Factor (Stress Ulcers): There is considerable evidence that supports the role of stressful life events in the etiology of PUD. Stress-induced ulcers are due to an increase in free radical generation apart from acid pepsin factors. Stress causes an increase in gastric motility, vagal overactivity, and mast cell degeneration, reducing gastric mucosal blood flow. Stress may also produce ulceration by the release of histamine with enhanced acid secretion and reduced mucous production. Cold-restrained stress-induced ulcers are the result of autodigestion of the gastric mucosal barrier, accumulation of HCl, and generation of free radicals.

Types of Peptic Ulcer

Based on location, peptic ulcers are categorized as follows:

  1. Gastric Ulcer: Occurrence of ulcer in the stomach, more commonly in older age group.
  2. Duodenal Ulcer: Occurrence of ulcer in the duodenum. They occur commonly in younger individuals and are evenly distributed among various socioeconomic groups. These patients have higher than normal levels of acid secretion rates. Depending on the severity, peptic ulcers are classified as:
  • Acute Peptic Ulcer: These ulcers involve tissues to the depth of the submucosa. They may arise in the form of single or multiple lesions. They are found in many sites of the stomach and the first few centimeters of the duodenum.
  • Chronic Peptic Ulcer: These ulcers penetrate through the epithelial and muscle layers of the stomach wall and may include the adjacent pancreas or liver. In the majority of cases, they occur singly in the pyloric antrum of the stomach and the duodenum.

Symptoms

The most common symptom of a peptic ulcer is abdominal discomfort. This discomfort comes and goes for several days of the week, generally occurring 2 to 3 hrs after a meal, in the middle of the night, when the stomach is empty. Other symptoms include blood loss leading to anemia, weight loss, poor appetite, bloating, burping, nausea, and vomiting. In patients with an advanced-stage emergency, symptoms are sharp, sudden, and persistent accompanied by stomach pain, bloody or black stools, blood in vomit, etc

ACUTE PEPTIC ULCER

They are usually multiple erosions due to disruption of the mucosal barrier.

Causes- Stress, drugs like analgesics, steroids, surgeries.

Clinical Features

  • Sudden onset of acute pain and tenderness in the epigastric region.
  • Vomiting with or without haematemesis.
  • Often acute peptic ulcers can lead to perforations.
  • Acute ulcers after cerebral trauma or neurosurgeries are called Cushing ulcers.
  • Acute ulcers after major burns are called curling ulcers.

Diagnosis is by gastroscopy.

Treatment

  • Intravenous ranitidine 50 mg, 8th hourly.
  • IV fluids.
  • Blood transfusions if there is bleeding.

Curling’s ulcers

They are acute ulcers that develop after major burns, presenting as pain in the epigastric region, vomiting, or haematemesis. Treatment is conservative- IV ranitidine. IV pantoprazole 80 mg in 100 ml DNS low, later 40 mg IV maintenance.

Note: curling ulcer occurs when burn injury is more than 35%.

Cushing ulcers

They are acute ulcers that develop after cerebral trauma or after neurosurgical operations. Treatment is conservative by IV Ranitidine. It is commonly a single, deeper ulcer that more frequently perforates. It can occur in the esophagus and duodenum also.

GASTRIC ULCER

Etiology

It occurs due to an imbalance between protective and damaging factors of the gastric mucosa.

  • Atrophic gastritis.
  • Smoking, alcohol.
  • Helicobacter pylori infection (70%).
  • There is either normal chlorhydria or hypochlorhydria.
  • Altered mucosal barrier mechanism.
  • Lower socioeconomic group.

Factors involved in Gastric Ulcer Formation

  •  Duodenal-gastric reflux containing bile salts and lysolecithin breaks the mucosal barrier making it more vulnerable to injury, the action of drugs, and pepsin injury.
  • Gastric stasis.
  •  Ischaemia of the gastric mucosa.

Types of Gastric Ulcer (Daintree Johnson)

Type          Location                                                                               Incidence                      Acid level

1      In the antrum, near the lesser curve                                                55%                       Normal

2  Combined gastric ulcer with duodenal ulcer                                   25%                       High

3     Prepyloric ulcer                                                                                 15%                         High

4    Gastric ulcer in the proximal stomach or cardia                           5%                             Normal

Note: Often in a lesser curve, saddle-shaped ulcers can occur.

Clinical Features

  • Equal in both sexes.
  • Pain in the epigastric region after taking food, lasting up to two hours. Pain is uncommon during the night. Relieved by vomiting or by inducing vomiting.
  • Periodicity: symptom-free intervals maybe 2-6 months. Often with seasonal variation.
  • Vomiting relieves pain.
  • Haematemesis and melaena: Haematemesis is more common.
  • Their appetite is good but hesitant to eat because eating induces pain and that results in loss of weight.

Differential diagnosis

  • Hiatus hernia
  • Cholecystitis
  • Chronic pancreatitis
  • chronic gastritis
  • dysphagia
  • carcinoma stomach

Investigations

  • Barium meal X-ray to see niche and notch.
  • Gastroscopy – for location, type of ulcer, and also to take a biopsy.
  • US abdomen mainly to rule out other diseases and to confirm the associated diseases.

Treatment

  • Drugs like H2 blockers, proton pump inhibitors, and carbenoxolone help in reducing or eliminating the symptoms but asymptomatic ulcers may exist silently and may turn into malignancy So surgery is the preferred line of treatment. Partial gastrectomy and Billorth I gastroduodenal anastomosis is done.
  • Type 4 proximal gastric ulcer is difficult to manage.

Complications of gastric ulcers

  • Hourglass contracture; which occurs exclusively in women is due to the cicatricial of lesser curve ulcers.
  • Tea-pot deformity: (Hand-Bag stomach) is due to cicatrization and shortening of the lesser curvature.
  • They present with features of pyloric stenosis.
  • Perforation.
  • Bleeding by erosion into the left gastric and rarely splenic vessels or to vessels in the wall of the ulcer.
  • Penetration posteriorly into the pancreas, anteriorly into the liver.
  • Malignant transformation is usually into adenocarcinoma of the stomach (2-5%).

Clinical features

  1.  Loss of periodicity.
  2.  Persistent pain.
  3.  Vomiting.
  4.  Loss of appetite and weight

Diagnosis

  • Barium meal: It shows filling only in the proximal stomach or double-pouched stomach.
  • Gastroscopy.

 Treatment

Partial gastrectomy wherein gastric ulcer with a lower compartment of the stomach is removed and Billroth-I anastomosis is done.

DUODENAL ULCER

Etiology

  •  Common in people with blood group O +ve.
  • Stress, anxiety hurry, worry, curry.
  •  Helicobacter pylori infection is an important etiology for duodenal ulcers (90%).
  •  NSAIDs, steroids
  •  Endocrine causes: Zollinger Ellison syndrome, MEN syndrome, hyperparathyroidism.
  •  Other causes: Alcohol, smoking, and vitamin deficiency.

Pathology

  1.  An ulcer occurs in the first part of the duodenum, usually within the first inch, involving the muscular layer.
  2. Sites: a. In the bulb (bulbar)95%.    b. Post bulbar (5%).
  3.  Eventually, it shows cicatrization causing pyloric stenosis. Serosa overlying the site of the duodenal ulcer shows petechial hemorrhages with speckled red dots, appearing like sprinkled cayenne pepper

Clinical Features

  •  In India, the ratio of duodenal ulcer to the gastric ulcer is 30: 1. A very high incidence.
  • It is common in all socio-economic groups, more with stressed professionals (Type A personality).
  • Pain is more before food, in the early morning, and decreases after taking food. Food relieves the hunger pain. Night pains are common.
  •  Common in males.
  •  Periodicity is more common than in chronic gastric ulcers with seasonal variation.
  •  Water brash, heartburn, and vomiting may be present.
  •  Melaena is more common, haematemesis also can occur.
  • Their appetite is good and there is a gain in weight.
  • It decreases once stenosis develops.
  •  Eats more frequently without any restriction.
  •  Chronic duodenal ulcers can be uncomplicated or complicated.

Differences between clinical features of gastric ulcer and duodenal ulcer

Gastric ulcer                                                                    Duodenal ulcer

Pain after food intake                                                     Pain before food intake

Periodicity less common                                                Periodicity more common

Haematemesis is more common                                        Malena is more common

Weight loss occurs                                                          Weight gain occurs

Equal in both sexes                                                         Common in males

No pain in empty stomach                                                 food realize pain [hunger pain]

Food never reduces pain                                                   Food reduces pain

No pain at night                                                                   Incidence of nocturnal pain

Vomiting is common so it releases the pain                  After taking he feels better so he takes a frequent diet

Tenderness left to the midline of EPG                                Tenderness at duodenal point

Complications of  Duodenal Ulcer

1. Pyloric stenosis: Due to scarring and cicatrization of the first part of the duodenum.

2. Bleeding (10%).

3. Perforation (5%). Both acute and chronic ulcers can perforate. Anterior ulcers perforate.

4. Residual abscess.

5. Penetration to the pancreas.

Investigations

Barium meal X-ray shows deformed or absence of duodenal cap (because of spasm). The appearance of trifoliate duodenum is due to secondary duodenal diverticula which occurs as a result of scarring of the ulcer.

Gastroscopy reveals the type, location of the ulcer, and narrowing if any.

Biopsy for the presence of Helicobacter pylori.

Estimation of serum gastrin level, and serum calcium level.

Treatment

I. General measures: Avoid alcohol, NSAIDs, smoking, and spicy foods. Have more frequent food.

II. Specific measures:

Drugs

  • H2 Blockers: Promotes ulcer healing in 4-8 weeks, by reducing acid secretion.
  • Proton pump inhibitors: Inhibit parietal cell H+, K+ ATPase enzyme responsible for acid secretion. . They stop acid secretion completely.
  • Antacids: Neutralises the HCl to form water and salt and also inhibit peptic activity.
  • Sucralfate is an aluminum salt of sulfated sucrose that provides a protective coat to ulcer craters, promoting healing. It inhibits peptic activity. The dose is 1 g qid for 6 weeks (Before food). It is an effective drug.
  • Anti-Helicobacter pylori regime: It is very useful, given for 7-14 days later the proton pump inhibitors are continued.
  • Colloid bismuth sulfate is a good drug for ulcers, but it stains the oral cavity and mucosa.
  • Misoprostol is the only prostaglandin agonist accepted. A Follow-up gastroscopy is a must, to confirm that the ulcer has healed.

Surgery for Uncomplicated DU

  •  Highly Selective Vagotomy (HSV).
  • Selective vagotomy with pyloroplasty (SV + P).
  • Truncal vagotomy with gastrojejunostomy (TV + GJ).
  • In HSV, only fibers supplying the parietal cells are ligated. The nerve of the Latar jet which supplies the antrum pump is retained and so no drainage procedure is required in HSV. HSV is also called parietal cell vagotomy or super-selective vagotomy. Here nerve fibers in the last 6 cm of the stomach, just proximal to the pylorus are preserved (Crow’s foot). A vagotomy reduces acid secretion, hence ulcer heals. No acid, no ulcer.
  • Posterior truncal vagotomy with anterior seromyotomy—Taylor’s operation. It can be done through laparoscopy.
Inflammatory Bowel Disease

Best Way to Mange Inflammatory Bowel Disease Through Ayurveda

by with One Comment Gastrology

Inflammatory Bowel Disease

Inflammatory Bowel Disease is psychosomatic and has a high risk due to a fast lifestyle and increased stress full life. In the past few decades, the prevalence of IBD has reached an alarming proportion among Indians. Inflammatory Bowel Disease comprises a group of o+ commoners in psychosomatic disorders that share the phenotype of abdominal pain, diarrhea, vomiting, rectal bleeding, and severe internal cramps/muscle spasm. The metabolic deregulation associated with Inflammatory Bowel Disease causes a secondary path of physiologic changes in the digestive system.

Ayurveda considers health and disease both as the products of food, lifestyle & Mansika bhava. Positive thinking and Mansika health prevent diseases. It is in tune with this concept that Ayurveda involved intensive Mansika health/Achar Rasayana, Dhi, smriti, etc. Such codes of life and health conduct relate to the personal, social as well as spiritual dimensions of an individual. It is amazing that thousand years ago, Ayurveda conceived the significance of the error of lifestyle in causations of all kinds of disease, both physical and mental now which is considered the principal cause of many illnesses prevalent today. Ayurveda provides a better solution in the form of proper dietary management, lifestyle advice like Ahara- vihara, yoga, Basti- panchakarma, and medication for better management of IBD

The psychosomatic term is known as the relation between psycho (mind) and soma (body). So Psychosomatic disorders are manifestations of physical imbalance in which emotional components have a strong influence. It is a condition of dysfunction or structural damage in bodily organs through inappropriate activation of the involuntary nervous system and the glands of internal secretion which resulting Skin eruption, heart disorder, metabolic disorder, and digestive disorders like IBD, PEPTIC ULCER, etc. IBD or Inflammatory Bowel Disease is characterized by ulceration in the bowel. Clinically manifest as blood and mucous in stool. Ulcerative colitis with Crohn’s disease comes under this heading. Hence Amoebic dysentery, Intestinal TB, and Enteric fever with intestinal manifestation can also include in this. IBD affects 11% of the population globally. Autoimmune factors, Psychosomatic, and Dietary factors are mainly responsible causative factors for IBD.

In Ayurveda Acharya has mentioned that Sharira doshas and Manasika doshas (psychosomatic) both are affecting Agni. Agni is important for Samyaka Ahara Pachana Kriya. They mentioned various types of Agni in which Mandagni is responsible for Atisara, Grahani, Fever, etc. Acharya Sushruta mentioned Grahani rog and Atisara in Shusruta Samhita Uttar tantra. IBD is treated in Ayurveda as Grahani rog and Raktaj and Shokaj Atisara after assessing the dosha predominance based on signs and symptoms by the Devprasrya and Yuktivipasrya Chikitsa for correcting the doshas involved in it.

Classification of IBD:

The two most common diseases are described under IBD

(1)Ulcerative colitis

(2) Crohn‟s disease

Diagnosis of IBD:

The investigation is colonoscopy/ sigmoidoscopy/ barium enema

Symptoms of IBD

Abdominal pain · Diarrhoea · Rectal bleeding · Severe cramps/ muscle spasm · Tenesmus

Complication of IBD

Acute Chronic
Toxic megacolon Carcinoma of the colon
massive hemorrhage Recurrent perianal abscess
Perforation protein malnutrition
rectal diseases

Management of IBD

Conservative Surgery
  • Hospitalization
  • Blood and fluid transfusion
  • Antibiotics
  • Steroids
  • Sedative & tranquilizers
  • Total proctocolectomy
  • Total colectomy

The drawback of modern therapy for IBD –

  • Steroids can harm CNS. They can produce diseases like cardiovascular disease, infertility, renal disease, and liver disease.
  • A long intake of antibiotics harms the digestive system and produces side effects.
  • Blood transfusion- Transferred infection, hemolytic reaction, etc.

IBS management by Ayurveda

IBD in Ayurveda

In Ayurveda, an exact correlation cannot be found of IBD, but according to signs & symptoms and pathology of the disease, it can be compared with Sangrahani (mild to moderate) and Raktatisar (severe stage) according to severity. Raktatisar is mentioned in Sushruta Samhita Atisarpratisedha‟ Adhyaya and its symptom like diarrhea with hemorrhage from the rectum, jwar, udarshool, Trishna, Daha, Vrana can be compared with rectal pain, inflammation, rectal ulceration, and bleeding per rectum of IBD. The description of Sangrahani is given by acharya Madhav in the textbook „Madhav Nidana‟. Symptom of Sangrahani is very much similar to those of the Mild to moderate stage of IBD as Antrakunjan relates with Tenesmus, Daurbalya to weakness and sadnam reflects the debility condition of the patient due to Aam bahu paichilyam stool along with mucous.

Etiology

The main causative factor of these diseases is Aam dosha and Vata-Pitta doshas. Mithya Ahara- vihara i.e; Samashana, Adhyashana, Vishamashana and not following the proper dietary rules (Astahar Vidhi viseshaytan) and vihara i.e.; Faulty food habits (Ahara Vidhi) associated with disturbed and stress full mind is responsible for mand Agni (Decreased quality and quantity of digestive enzymes), which is the main causative factor for producing aam dosha and in vitiation of Vata-pitta doshas.

Characteristic of Sangrahani and Raktatisar

Sangrahani: Antrakunjan, Alashya, Daurbalya, Kativedna, Shit(cold)- draw(liquid)-ghan(semisolid)-Snigdha(oily) stool with mild pain.

Raktatisar: Diarrhoea with hemorrhage, jwar, udarshool, Trishna, Daha, and vran(ulcer).

Complication of Sangrhani and Raktatisar –

Soth -Kaas -Chardi -Jwar -Swash – Murch -Trishna-Arochak -Hikka -Pandu -Gudabhransh

Line of treatment

Ayurveda is broadly divided into two parts; Devprashrya(mantra) and Yuktiprashrya (Ahara-Vihara and Aushadha karma).

Nowadays Devprashrya Chikitsa is well known as Spiritual karma (mantra tapa etc) and Yuktiprashrya is Ahara-vihara karma and Samashana and Sodhana(panchakarma) chikitsa, where Spiritual karma act over Mansika doshas by prabhav guna.

Chikitsa:

· Nidan parivarjan: by following dincharya and Ritucharya.

· Samshan: · Deepan- Pachan aushad-Chitrakadi vati.

· Snehan: changeryadi ghrat, local massage of saindhav with tail

· Sanghrahi: kapithastak churna, Bilvadi churna

· Vasti: Picha vasti

· Yoga: Pranayam, Vajrasan, mayurasan, bandh-karma, Jal kunjan.

Pathya / what to eat Apathya / what to avoid
Laghu(light), Supachaya (easily digestible) deepan-paachan(digestive)ie; Moong, masoor, moth, arhar indar jau, ghee, nimbu, anaar, makhana, Yoga, and Pranayam Guru(heavy), Abhisyandi(cause of channel blocker), ushan(hot), tiksn- aahar- vihar i.e; mash(pulse), mash(meat), tail,mirch-  masala‟s

Discussion: Picha Basti is considered best among all of the Basti by Acharyas for the Treatment of Sangrahni, Raktaatisara.

CONTENTS OF PICHA VASTI:

Makshika – 250 ml

Saindhav Lavana – 2 gm

Sneha ( Changreyadi Ghrit + Shatadhauta Ghrit) – 125 ml+125 ml

Kalka ( Mulethi Churna ) – 30 g

Kwath ( Salmali Niryasa and Mustadi Ksheer) – 200 ml

Mode of action of Picha vasti:

  • Picha Basti is Pichhila (sticky or lubricant) and Agnideepaka in nature (due to its content).
  • In ulcerative colitis, the intestine gets inflamed and sensitized, and when food passes through the intestine and makes contact with the mucosa of the intestine it gets irritated.
  • It is said that Basti should be administered to the patient lying on the left lateral side as the Grahani and Guda are situated on the left side of the body, and the valves of the Guda get relaxed, in this position Basti drugs reach up to the Grahani due to Vyavyi and Vikasi Guna of Saindhav lavana.
  • It forms a protective film over the intestine, avoids friction over mucosa, inflammation subsides and mucosa becomes normal.
  • Agni Deepak property of Picha Basti helps in the ignition of the Agni (Grahani is the main seat of Agni) so that absorption and digestion of Basti over the colon takes place effectively.
  • Simultaneously Picha Basti which also has Sangrahi properties reduces the bowel frequency and there will also be no loss of electrolytes and enteropathy protein (prevent hypoalbuminemia state).
  • Honey and Saindhav Lavana colloidal solution along with Sneha form an impervious coating over the entire colon. There will be no loss of electrolytes and prevent the direct attack of inflammatory mediators on the mucosa, thereby reducing the inflammatory process and facilitating healing.

CONCLUSION:

In inflammatory bowel disease in which Psychosomatic factors play role in the progression of the disease, Ayurvedic treatment rapidly heals the inflamed ulcer area. Simultaneously have a mind relaxation effect without having an ill effect on health and also prevents remissions.

In the present era‟ Ayurveda is a good treatment modality of IBD as it reduces stress by Devprashrya and Yoga karma Reduces inflammation by Picha-vasti and Agni –Deepak drugs by forming an impervious coating over the entire colon.

So it can be concluded that Ayurveda provides a better solution in the form of proper dietary management, lifestyle advice like –Panchakarma (detoxification and bio purification procedures), meditation, yoga-like- Padmasan, shavasan, etc are better managed in Sangrahani and Raktatisar (IBD).

Author

Dr. Neeraj Sharma

Ph.D. (AYU), M.S(Shalya)

AYURKAUSHALAM
Serving for Health & Education New Delhi & Jodhpur.

Consult for – ANORECTAL DISEASES, BPH, and Renal Stone disease.

Wound and Pain management

Mail- ayurkaushalam@gmail.com

Contact. 7231053235

Fissure

Basic Fundamentals of Fissure in Ano as per Ayurveda

by with No Comment Gastrology

Fissure

Fissure is described in Sushrut Samhita. It is described in the complications of Garbini (pregnant lady) in the Kashyap Samhita, Khilasthana. Parikartika resembles a fissure‑in‑ano having cutting and burning pain at Guda. Acharya Sushruta mentioned it as one of the complications in the Virachanaa (purgation therapy) and Vasti karma (enema therapy). Acharya Charaka described it in vyapad of vaman-virechan and Basti Vyapad (a complication of medicated enema), and Bastinetra Vyapad (a complication of medicated enema tube).

DEFINITION:

Parikartika or Parikartana. Vyutpatti: The word Parikatika consists of two words. Pari- around, about; Kartana- the act of cutting off; Krintati– clip, cut off. Nirukti: Unbearable cutting type of pain all around Guda, Bastishiras, and Nabhi is termed Parikartika.

ETIOLOGY :

 Diet-related etiology :

Diet plays a very important role in Parikartika which is evident from references. Vagbhata and Kashyapa have explained that intake of Mudga, Kodrava, Chanaka, and other pulses and Rooksha charas which is water absorbent in nature (Sangrahi) lead to constipation. Apanavata gets aggravated in its seat (Pakwashaya) which blocks the adhovaha srotas, dries them up (of their moisture), and produces obstruction to the movement of feces, flatus, and urine by which Parikartika occurs 8&9. As per modern science intake of nonfibrous food will lead to the hardening of stools and cause Fissure-in-ano.

            When Vata is covered with feces, the stool is constipated, the patient suffers from severe pain and passes hard stools with difficulty, and evacuation is delayed. This causes Parikartana leading to Parikartika. If a person is debilitated with Mridukoshta or Mandagni, the ingestion of Atirooksha, Atiteekshna, Atiushna, Atilavana Sahara causes Dushana of Pitta and Anila and produces parikartika.

 Disease-Related etiology :

  • Udavarta (Purisajaudavartaor Purisavrta Vata)
  • Arsha (Prodromal features and symptoms of Vatika and Kaphaja Arsha) – Abnormality of the internal sphincter predisposes the patient to the formation of both hemorrhoids and fissures.
  • Jirnajwara
  • Vatika Atisara
  • Vatika Grahani

Physician related etiology :

  1. Vairocana Vyapada – A person having Mrudu Kostha and Alpa Bala ingest Tiksna, Ushna, and Ruksa drugs for Virechana, then this disease results.
  2. Vasti Vyapada (niuruha)- If Ruksa Vasti containing Tiksna and Lavana drugs is administered in heavy doses; it may produce Parikartika.
  3. Excessive use of Yapana Vasti – It may lead to Parikartika along with other diseases.
  4. Vasti Netra Vyapada – Due to inappropriate administration of the enema nozzle and defects in the enema nozzle itself may cause this disease.

SAMPRAPTI :

In the concerned disease, the predominant vitiated Dosha is Vata. Dushya is Twak, Rakta, and Mamas, specifically in Guda Pradesh, which affects gradually according to the progress of the disease. The Vyana Vayu when obstructed by the pathway of Apana Vayu led to the formation of Parikartika associated with Udavarta. Due to the etiological factor, there is Dusti of Purisavaha Srotas. When Purusha is obstructed the natural way of Apana Vata also causes vitiation of Vayu. As a result of the pathogenesis, when Vata localizes in Twak, it becomes Ruksa and shows a tendency to crack. As the disease progress, the vitiated Vayu is localized in Rakta, and the formation of an ulcer takes place. Thereafter when it localizes in Mamsa forming knotty swelling or tags and pain. Though there is a predominance of Vayu, it is associated with Pitta (according to Acharya Sushruta) and Kapha (according to Acharya Kasyapa)

Another Samprapti is due to Agantuja Nidana where there is wound formation in the first stage and then the Doshas get sited in the Vrana, producing further symptoms. When the wound is produced simultaneously there is vitiation of Dosha which in term leads to Parikartika.

LAKSHANA/SYMPTOMS:

The terminology Parikartika is itself representing the symptom, which is the intensity of pain. It is a sharp cutting or sawing type of pain. It’s severe pain with bloody mucous discharge associated discomfort in the perianal region as per Charaka. The pain persists before and after defecation mentioned by Susruta. There is vitiation of Vayu mainly the Purisavrta Vata. The involvement of Dushya as a disease concern will be Twak, Rakta, and Maṃsa. When vitiated Vayu affects the following Dhatus, symptoms become more relevant as per disease concern.

SADHYASADHYATA/PROGNOSIS :

Generally, Vrana in Payu is easily curable. If a Vrana is left untreated, as a consequence it may lead to the Yapyatwa stage and finally leading to the Asadhyatwa stage. Parikartika which affects the superficial layer of the Twak (anal skin) is easily curable in a short time. Therefore it can be included in the Sukhasadhya group. If it affects the deeper layers, it deals with wound healing. And if it is associated with Madhumeha, Kustha, Vishodusti, and Sosha, the healing of Vrana will be delayed. If Parikartika is associated with Sanniruddha

Guda, is considered as Yapya.

In Astanga Samgraha some Arista Lakshana is mentioned about Parikartika.

a) When Parikartika is formed due to Amasaya cause and associated with severe thirst and Sakrutabheda.

b) When Parikartika is formed due to Pakwasaya cause and associated with severe thirst and Gudagraha.

CHIKITSA/TREATMENT :

The Mandagni is a most important factor in Parikartika as well as in Arsha, Atisara, and Grahani. So increasing and maintaining the Agni in an equilibrium state is necessary. Up to 70 % of acute fissures resolve with conservative medicine, if not they progress to form a chronic fissure. However, Ayurvedic preparations are used in the primary stage of the disease the chance of progression in chronic one can be minimized. The main aim of treatment is to relieve sphincter spasms and heal fissure wounds, soothe the anal canal, and relieve the agonizing pain and associated burning sensation and bleeding.

  1. Nidana Parivarjana (removal of etiology)- It is the first step of treatment.
  2. Avagahana-sweda (Hot fomentation- Sitz bath): Sitting in a warm/hot water tub after each bowel movement soothes the pain and relaxes the spasm of the internal sphincter for some time.
  3. Local application of Durvadya tail–  Main ingredient of Durvadya tail is Durva (Cynodondactylon), Kampillaka (Mallotus philippensis), Daruharidra (Berberis aristata), and Til tail (sesame oil).
  4. Matra Basti (type of Anuvasana Basti): It acts as a retention enema and helps in the easy voiding of stools, by this Vatanulomana occurs and it cures the diseases caused by aggravated Vata as Parikartika is Vata dominate Vyadhi. By giving Matrabasti local Snehan occurs, the spasm will also be relieved and thus brings down the pain. It softens the stools, lubricates the anal canal, and provides an easy evacuation.
  5. High fiber diet: The rate of intestinal passage of food depends on the nature of the diet and its fluidity. The greater the indigestible residue and water content, the more rapidly it reaches the rectum and produces its distension and thereafter evacuation. Hence patients should take daily fiber-rich food and plenty of fluids to improve digestion and regularize their bowels. These are hygroscopic, which allows them to expand and become mucilaginous. These fibers are a complex carbohydrate, which binds with water in the colon creating larger, softer, stools. Larger, softer, stools stretch and relax the sphincter muscles helping the blood to flow and it also requires little pressure to pass.
  • In the Jwara Chikitsa, Acharya Charaka has also mentioned that in Jwarita person, there are chances of having Parikartika. He should consume Peya of red rice made from decoction of Vrakshamala, Badara, Pithivana, and Kantakāri with powder of unripe fruit of Bela’s cortex.
  • About Garbhini Chikitsa, Acharya Kasyapa classified the disease into three categories and gave specific treatment according to the Doshic involvement.
  • Taila/Ghrita Pichu: It forms a protective layer over the fissure wound, it smooths the anal canal and relieves pain by releasing sphincter tone and cleaning the wound thus helping in the healing of ulcers.

CHIKITSA FOR SHUSHKARSH / BAHYARSH :

In Ayurvedic text information available on Shushkarsha, Bahyarsha can be correlated with Sentinel Piles. Acharya Sushruta mentioned four modalities of management

1) Bheshaja (conservative line of management)

2) Kshara

 3) Agni 

4) Shastra. 

In kshar chikitsa, kshar sutra ligation was done to sentinel piles. of this themselves they may fall within a few days. Also can use as Lepa of  Pratisaraneeya kshara is done over the (Chronic fissure-in-ano) ulcer surface, by lekhan karma of Kshara, this reduces the excess fibrous tissue present over the ulcer surface and the ulcer heals & sphincter relaxation occurs simultaneously.

DISCUSSION :

Based on location, nature of pathology, and features, Gudaparikartika can be correlated to Fissure-in-ano. The detailed description of Nidana (etiology), Samprapti (pathogenesis), Lakshana (symptoms) & Chikitsa (treatment) is mentioned in Sushruta Samhita, Kashyapa Samhita, Astanga Hridaya, etc. There is a detailed description of conservative and surgical treatment for Fissure-in-ano.

CONCLUSION :

  • Improper dietary regimens and stressful life are found to have influenced the high incidence observed today. 
  • Passage of hard constipated stools is the prime cause of tears in the lower anal canal which results in excruciating pain during and after defecation, the cardinal feature of Fissure-in-ano.
  • Ayurvedic preparations are all effective & these can cure fissures and regularize bowel in up to 90% of cases of acute fissures. These could always be offered to patients who are not willing to operative procedures such as cardiac patients or patients with diabetes, AIDS, or Hepatitis B where healing is difficult after the operation.
  • Kshara is used in different forms like Kshara Lepa, and Ksharasutra ligation in treating Parikartika (Chronic Fissure-in-ano).