Pravahika: Dysentery

The vayu in the organism of a person addicted to the use of unwholesome food is deranged and aggravated. It carries down the accumulation of mucus into the lower part of the body, where, mixed with stools, it is constantly passed with tenesmus. The disease is called pravahika (dysentery).” (1)

In this article we will consider dysentery, known as pravahika, from the standpoint of modern Western epidemiology. In India, the main causes of pravahika would be amoebic dysentery and bacillary dysentery. Currently in the West, a majority of dysenteric illnesses relate to inflammatory bowel disease (IBD): Crohn disease, ulcerative colitis, and microscopic colitis.

Sushrut includes pravahika or dysentery in the chapter on atisar, diarrhoea. Madhavacharya follows Sushrut in this. Vagbhat and Charak mention pravahika in their sections on treatment of vata atisar.  But specifically, dysentery involves the anubhandan or conjunction of kapha and vata atisar. “Vata gets increased and associating with kapha produces the disease called pravahika” (2).

Symptoms of pravahika include frequent elimination, often of small quantities of faeces, mucus in stools and tenesmus. The small quantity is accounted for by the fact that mucus is extremely irritating and can trigger an urgent call to stool simply to pass some mucus or a small amount of mucus-filled stool. As described in the classical texts, pravahika is characterized by bahusam (frequency), alpalapam (small quantity), sashulam (with pain), sapravahikam (straining i.e. a very intense urge again caused by the irritant effect of mucus), saraktam (blood in stool), sapicham (jelly-like mucus), upveshayte (urgency of defaecation) (2).

Vataj pravahika is characterized by frequent defaecation accompanied by pain, a typical symptom of Crohn Disease. Pittaja pravahika is accompanied by burning sensation, kaphaj pravahika by mucus in stools, common in amoebic dysentery and raktaj pravahika with blood in the stools, as in the case of ulcerative colitis (2).

Crohn disease is a typical form of vataj pravahika, since its main symptoms are dysentery and pain. In addition, the course of the illness is unpredictable (3), a typical vata quality. The disease affects the small intestine, particularly the terminal ileum, as well as the ascending colon (3).  Thus as it progresses it can lead to malabsorption as well as to small bowel obstruction and abscess formation. Secondary conditions resulting from fat malabsorption include steatorrhoea (fatty diarrhea), fat-soluble vitamin deficiency, gallstones, kidney stones, clotting disorders and osteoporosis (4). The causes include a genetic khavaigunya in the digestive tract along with dietary and lifestyle factors, notably a high fat diet and smoking. In our clinical experience, a combination of a high-fat junk-food diet of pizza, burgers and fries, accompanied by smoking, is often a prelude to Crohn Disease in susceptible subjects (5). Crohn Disease typically begins in young people between the ages of fifteen and thirty. (4) It occurs with increased frequency in Ashkenazi Jews (6).

Ulcerative colitis (UC) is a type of raktaj pravahika, characterized by rectal bleeding, mucus discharge from the rectum and frequent stools. Tenesmus may also occur. Unlike Crohn disease, it is confined to the large intestine, beginning in the rectum and spreading into the rest of the colon. UC is three times more common than Crohn disease (7). It frequently begins in young people aged 15-25 although onset can occur at any age (8). Like Crohn disease, it is more common in Ashkenazi Jews. An autoimmune condition, UC may be associated with autoimmune disorders outside the digestive tract. Up to 6.2% of patients with UC have such manifestations, which include autoimmune eye disease (uveitis), ankylosing spondylitis, inflammatory back pain and sclerosing cholangitis (9). Primary sclerosing cholangitis is a severe autoimmune liver disease leading to jaundice and liver failure and is found mainly in patients with IBD (10). Genetics (11), diet and stress (12) play a role in the development of UC. A pittagenic diet high in sulphur, as found in heavy consumption of red meat and alcohol, is associated with increased likelihood of relapse (13).

Micropscopic colitis includes both collagenous colitis and lymphocytic colitis (14). This milder form of colitis presents as atisar or diarrhea and lacks the typical features of pravahika. Indeed, microscopic colitis is often misdiagnosed as diarrhea dominant irritable bowel syndrome, although it is actually a mild form of IBD.  The colloidal colitis form of microscopic colitis is twenty times more common in women than in men (15). Microscopic colitis occurs more commonly over 40, peaking in the sixth and seventh decades of life, and should be considered in the differential diagnosis of atisar (diarrheal disease) in older women (16). Most if not all patients with microscopic colitis have lived for decades with undiagnosed coeliac disease (17). These patients respond extremely well to a gluten free diet, usually getting complete remission of symptoms when this diet is used in tandem with Ayurvedic herbs.

Treatment of pravahika is carefully described in both Sushrut and Vagbhat. Diet is of course of great importance since the condition arises due to use of unsuitable diet. During an acute episode, diet begins with rice gruel seasoned with cumin (18). When solid food can be taken, the first food is rice with curds or yoghurt (19). After this, soups, kitchari and boiled rice with rock salt and ghee can be given. Once the condition is in remission, patients with Crohn disease (vataj pravahika) can take a vata soothing diet while carefully avoiding trans fats and deep-fried foods. They should also be counseled to quit smoking. Patients with UC should adopt a vegetarian or semi-vegetarian pitta-soothing diet, avoiding alcoholic beverages. They should be instructed in relaxation and meditation techniques to manage their stress. Patients with microscopic colitis should adopt a gluten free diet regimen tailored to their constitution

Herbs can be used both rectally and orally. Sushrut mentions the use of picchila vasti with licorice powder, unpasteurized boiled milk, Salmali stems (silk cotton tree), kusha grass and ghee (20). Today, licorice ghee vasti can be used as a simplified version and in our clinical experience has proved highly effective in ulcerative proctitis and UC, due to the ropan or wound-healing properties of licorice (21). Vasti with a decoction of dashamula will relieve pain in the case of painful tenesmus (20).

Takram or buttermilk is the ideal vehicle for oral herbs during episodes of pravahika (22). When rectal bleeding is present, arjuna, both haemostatic and ropan (wound healing) can be used in takram (23). Other astringents herbs favored for dysentery include bilva ( 24) and kutaja (25). Ajwain, black pepper and ginger are used to stimulate normal agni (25). Triphala in small amounts (pinch size) is also effective in dysentery because of its astringency (22). As well as these herbs and remedies for use during the acute phase, guggulu is extremely valuable for maintenance and relapse prevention. Guggulu blocks pro-inflammatory gene expression, thus addressing IBD at the profound level of epigenetics (26). Because guduchi is anti-inflammatory and anti-spasmodic (27), the best guggulu formulation for IBD is Kaishore Guggulu. Therefore, in the absence of contra-indications, Kaishore guggulu should be continued long term in patients with IBD. Due to the autoimmune aetiology of IBD, shodhan therapies such as pancha karma should be effective to maintain remission and prevent relapse (28).

As we have seen, IBD is a disease of Western lifestyles, linked to consumption of high-fat, high meat diets, junk foods and stress (29). The Ayurvedic texts have considered mainly tropical diseases under the heading of pravahika. Yet Crohn disease, UC and microscopic colitis fit well into the descriptions of vataj pravahika, rakta pravahika and atisar, respectively. Furthermore, the traditional treatments for these conditions offered in the texts remain highly effective today, accompanied by lifestyle modifications. Due to the persistent and relapsing nature of IBD, maintenance therapies are also necessary in the long term.

1. Bishagratna KL tr, Sushrut Samhita, Chowkhamba Sanskrit Series, Varanasi, 1981 ut XL 82-83

2. Srikantha Murthy KR tr. Madhava Nidhanam, Chaukhambha Orientalia, Varanasi Ch 3 v 21-22.

3. Farmer RG, Hawk WA, Turnbull RB Jr. Clinical patterns in Crohn’s disease: a statistical study of 615 cases. Gastroenterology. Apr 1975;68(4 Pt 1):627-35.

4. Kornbluth A, Sachar DB, Salomon P. Crohn’s disease. In: Feldman M, Scharschmidt BF, Sleisenger MH, eds. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management. Vol 2. 6th. Philadelphia, Pa: WB Saunders Co; 1998:1708-34.

5. Kornbluth A, Sachar DB, Salomon P. Crohn’s disease. In: Feldman M, Scharschmidt BF, Sleisenger MH, eds. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management. Vol 2. 6th. Philadelphia, Pa: WB Saunders Co; 1998:1708-34.

6. Duerr RH. Update on the genetics of inflammatory bowel disease. J Clin Gastroenterol. Nov-Dec 2003;37(5):358-67.

7. Garland CF, Lilienfeld AM, Mendeloff AI, Markowitz JA, Terrell KB, Garland FC. Incidence rates of ulcerative colitis and Crohn’s disease in fifteen areas of the United States. Gastroenterology. Dec 1981;81(6):1115-24

8. Jang ES, Lee DH, Kim J, Yang HJ, Lee SH, Park YS. Age as a clinical predictor of relapse after induction therapy in ulcerative colitis. Hepatogastroenterology. Sep-Oct 2009;56(94-95):1304-9.

9. Bernstein CN, Blanchard JF, Rawsthorne P, Yu N. The prevalence of extraintestinal diseases in inflammatory bowel disease: a population-based study. Am J Gastroenterol. Apr 2001;96(4):1116-22.

10. Cox KL, Cox KM. Oral vancomycin: treatment of primary sclerosing cholangitis in children with inflammatory bowel disease. J Pediatr Gastroenterol Nutr. Nov 1998;27(5):580-3.

11. Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. Nature. Jul 26 2007;448(7152):427-34.

12. Levenstein S, Prantera C, Varvo V, Scribano ML, Andreoli A, Luzi C, et al. Stress and exacerbation in ulcerative colitis: a prospective study of patients enrolled in remission. Am J Gastroenterol. May 2000;95(5):1213-20

13. S L Jowett, C J Seal,  M S Pearce Influence of dietary factors on the clinical course of ulcerative colitis: a prospective cohort study Gut 2004;53:1479-1484

14. Baert F, Wouters K, D’Haens G, Hoang P, Naegels S, D’Heygere F, et al. Lymphocytic colitis: a distinct clinical entity? A clinicopathological confrontation of lymphocytic and collagenous colitis. Gut. Sep 1999;45(3):375-81

15. Margret Agnarsdottir, Olafur Gunnlaugsson, Kjartan B. Orvar, Collagenous and Lymphocytic Colitis in Iceland Digestive Diseases and Sciences  Volume 47, Number 5, 1122-1128

16. Fernandez-Banares F, Salas A, Forne M, Esteve M, Espinos J, Viver JM. Incidence of collagenous and lymphocytic colitis: a 5-year population-based study. Am J Gastroenterol. Feb 1999;94(2):418-23

17. Matteoni CA, Goldblum JR, Wang N Celiac disease is highly prevalent in lymphocytic colitis. J Clin Gastroenterol. 2001 Mar;32(3):225-7

18. Bishagratna op cit ut XL 90

19. ibid 87

20. Bishagratna op cit ut XL 84-86

21. Tuhin Kanti Biswas, Biswapati Mukherjee Plant Medicines of Indian Origin for Wound Healing Activity: A Review The Journal of Lower Extremity Wounds  2003 2, 1, 25—39

22. Ashtanga Hridayam chi IX 25-28

23. Rethinam Sundaresan Devi, Shoba Narayan, Ganapathy Vani, Gastroprotective effect of Terminalia arjuna bark on diclofenac sodium induced gastric ulcer Chemico-Biological Interactions Volume 167, Issue 1, 5 April 2007, Pages 71-83

24. Ashtanga Hridayam chi IX v 23- 25

25. Bishagratna op cit ut XL 92

26. Cheon JH, Kim JS, Kim JM, Kim N, Jung HC, Song IS (2006) Plant sterol guggulsterone inhibits nuclear factor-kappaB signaling in intestinal epithelial cells by blocking IkappaB kinase and ameliorates acute murine colitis. Inflamm Bowel Dis 12:1152-1161.

27. Avnish K. Upadhyay, Kaushal Kumar, Arvind Kumar Tinospora cordifolia (Willd.) Hook. f. and Thoms. (Guduchi) – validation of the Ayurvedic pharmacology through experimental and clinical studies Int J Ayurveda Res. 2010 Apr-Jun; 1(2): 112–121.

28. Ram Harsh Singh Exploring Quantum Logic in Ayurveda with special reference to Srotovijnana of Ayurveda Ayu-Vol.30,No.4(October-December)2009, pp.360-368

29. Yang, S.-K., Loftus, E. V. and Sandborn, W. J. (2001), Epidemiology of inflammatory bowel disease in Asia. Inflammatory Bowel Diseases, 7: 260–270. doi: 10.1097/00054725-200108000-00013