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Traditional naturopathic management of acute pancreatitis: a case study.

Introduction

Acute pancreatitis is a serious medical condition typically presenting to hospital emergency departments and carries with it a high mortality rate. It is considered a serious pathophysiological condition as once the pancreas is injured it can release lytic enzymes that can both enter the blood (causing severe shock) and also cause tissue digestion of the surrounding architecture. (1) Over 80% of hospital admissions associated with acute pancreatitis are attributed to biliary tract disease and acute alcohol consumption, (2) with the remaining causes being summarised in Table 1.1.

The incidence of acute pancreatitis is rising by 5% per year in the US and Europe, believed largely to be due to the increased presentation of biliary pancreatitis, (4-5) with 1/5 of these patients developing necrotizing pancreatitis, which exhibits a 10-30% mortality rate. (6) This high mortality rate is largely due to infection of the necrotic pancreatic tissue and represents the consequences of mucosal barrier failure, small bowel overgrowth and an inflammatory response leading to bacterial translocation of intestinal flora. (7-8)

Acute pancreatitis should be a clinical consideration for all patients presenting with acute abdominal pain. (2) Differential diagnoses associated with acute pancreatitis include perforated gastric or duodenal ulcer, dissecting aneurysm, appendicitis, diverticulitis, intestinal obstruction (strangulating), mesenteric infarction, biliary colic and an inferior wall myocardial infarction. (2) Signs and symptoms commonly experienced include severe abdominal pain, which may radiate into the back in 50% of cases (2) due largely to retroperitoneal involvement (3) and can require parenteral analgesia. The pain is classically steady, boring and unrelenting. The patient appears acutely ill and is typically sweating and may have diminished sensorium. (2) Nausea and emesis are common presentations with 20% of patients also experiencing upper abdominal distension, (2) rigidity and tenderness upon physical examination. The patient may present with either hypertension or hypotension with associated tachypnoea. Fever may be present and investigations typically reveal a raised WBC count. (2) While such cases are highly unlikely to present to naturopathic or herbal clinics due to the acute nature of the illness, should this occur, immediate transfer to an acute medical facility is an urgent priority.

Case presentation

The patient is a single 64 year old Caucasian male weighing 95.25kg (210 lbs) and measuring 175.26cm (69 inches) tall (BMI of 31), working as a primary healthcare professional (nurse practitioner) in California, USA. He works 6 days a week in clinical practice and is highly stressed and overworked due to keeping up with financing a mortgage, student loans and two dependents of university age. His diet is inconsistent but generally focuses on irregular meals of predominantly meat and vegetables, sugar-free diet sodas and other processed foods. Whilst physically robust, his exercise is also irregular due to working late hours, but usually consists of nightly walks after work with his dog of between 4-6 kilometres in a local nature reserve. Recreational drug use is limited to cigarette smoking (1 per day) and occasional alcohol consumption. He consumes coffee daily in the morning.

Medical and medication history

He has a previous medical history of familial mixed hyperlipidaemia (controlled with Crestor [rosuvastatin calcium] 20 mg qd), gastro-oesophageal reflux disease (controlled with Nexium [esomeprazole magnesium] 40 mg qd) and a recent bout of nonspecific prostatitis treated with Cipro [ciprofloxacin] 500 mg BID for the previous 7 days on a 14 day course. More recently he has undertaken treatment for depression (well controlled on Wellbutrin [bupropion] 150 mg sustained release BID) which had greatly improved his mental health. He was also diagnosed in 2013 with pulmonary fibrosis and was prescribed Symbicort (budesonide 160mcg/formoterol fumarate dehydrate 4.5mcg per pressurized metered dose) BID (q 12 hours) and an over the counter probiotic (20 billion organism count) BID since being on the ciprofloxacin.

Primary complaint

26/12/2014

The night before the presentation of symptoms, the patient was visited by his brother and consumed approximately 8 shots (240mL) of whiskey over a three-hour period. The patient's brother consumes alcohol regularly and is tolerant to such an amount; however, the patient is not a regularly consumer of alcohol and denies being overly inebriated during this time. The two consumed freshly caught red snapper fried in peanut oil, a salad and yellow rice as an evening meal with the patient retiring several hours later without any symptoms.

27/12/2014

The patient awakened at his normal waking time of 4:00 am. He put on percolated coffee and went out and sat for approximately 30 minutes in his outside hot tub. The temperature of the tub was 38.34C (101 degrees Fahrenheit) and the outside temperature was -1C (30 degrees Fahrenheit). The patient noticed a dull, constant pain in the epigastric region and upper left abdominal quadrant (4/10) at this time. The pain was associated with waves of nausea. The patient, who is a nurse practitioner, took Zofran ([ondansetron] 8mg oral disintegrating tablet) and then returned to his bedroom and took a nap without eating anything for breakfast. When he awakened an hour later the pain and nausea was more intense (7/10) and he had the urge to "burp" continuously in an effort to relieve the pressure. He took 30 mL of Mylanta (aluminium hydroxide 200mg, magnesium hydroxide 200mg & simethicone 20mg) without any improvement in symptoms. He was concerned he might be having an inferior wall myocardial infarction, so decided that at this point he needed medical assistance and chose not to drive 6 kilometres to the local hospital but rather 1 kilometre to one of the hospital satellite clinics nearby.

Shortly after arrival to the clinic the patient began vomiting green fluid that he described as not as bitter as one would expect after not eating for 12 hours. He was admitted to the clinic and an IV of normal saline was run and a blood draw completed. Presenting blood pressure was 108/60 with a pulse of 92bpm and a temperature of 37.2C (99 degrees Fahrenheit). The patient was also given a 12 lead electrocardiogram which ruled out any acute cardiac issues. He was administered promethazine 12.5 mg IV for his nausea and the effect was sedating. The patient was given 2 litres of normal saline over a two-hour period.

The lab studies included a CBC (Full Blood Count), Comprehensive Metabolic Panel, serum amylase, lipase and Troponin 1. The results of the lab investigations were as follows:
Haematology test results

Test             Test result   Reference range (^)

WBC              11.0 *        3.6-10.2 K/mm3
RBC              5.3           4.1-5.6 M/mm3
HGB              16.5 *        12.5-16.3 gm/dl
HCT              48.1 *        36.7-47.1%
MCV              91.3          73.0-96.2 fl
MCH              31.4          23.8-33.4 pg
MCHC             34.4          32.3-36.0 g/dl
RDW              13.1          12.1-16.2 %
MPV              7.9           7.4-11.4 fl
Platelet count   217           152-348 K/mm3

(^) Values and measurements consistent with
ranges set in the United States of America.

* Abnormal range detected

Troponin blood test

Troponin 1   <0.012   0.000-0.034 ng/mL

Diagnostic interpretation of data (^)

<0.034 ng/mL        Within normal range
0.034-0.120 ng/mL   Above upper reference limit
>0.120              Above MI diagnostic cut off

(^) Values and measurements consistent with
ranges set in the United States of America.

Comprehensive Metabolic Panel

Test name           Test result   Reference range (^)

Glucose             106           61-114 mg/dL
BUN                 22            6-22mg/dL
Creatinine          1.0           0.7-1.3 mg/dL
Sodium              136           135-143 mEq/L
Potassium           4.5           3.4-5 mEq/L
Chloride            102           98-108 mEq/L
CO2                 25            22-30 mEq/L
Calcium             9.4           8.6-10.2 mg/dL
Corrected calcium   9.0           8.6-10.2 mg/dL

Calcium result corrected for serum albumin

Bilirubin, total    0.9           0.1-1.4 mg/dL
Alk phosphatase     67            62-130 U/L
AST (SGOT)          30            16-63 U/L
ALT (SGPT)          56            21-72 U/L
Total protein       7.3           6.3-8.3 gm/dL
Albumin             4.5 *         3.6-4.4 gm/dL
Globulin            2.8           1.8-4.0 gm/dL
Alb/Glob Ratio      1.6           N/A
BUN/Creat Ratio     22.0          N/A
GFR                 >60           <60 Chronic renal disease
                                  <15 renal failure
Lipase              377 *         23-300 U/L
Amylase             114 *         32-108 U/L

(^) Values and measurements consistent with
ranges set in the United States of America.

* Abnormal range detected


Investigations

Based on these results and history, the attending physician diagnosed classic acute pancreatitis and discharged the patient with instructions including 1 week off work and no alcohol. No imaging or ultrasound was ordered to investigate for gallstones or pseudocyst and no medications were prescribed at this time with the patient being advised to return if symptoms did not ameliorate or if pain became excessive.

Following discharge, the patient was very sedated from the promethazine and had an altered state of consciousness, but managed to drive home to his residence. He slept for the next 36 hours only getting up to drink fluids and void. He got up feeling slightly improved but still complaining of upper left abdominal pain (6/10). Over the next 12 hours the patient developed intermittent abdominal cramps (pain 7/10) and diarrhoea associated with high fever (39.5C) and delirium. Treatment of the fever with 440 mg of naproxen sodium was hindered by lack of absorption due to hypermotility.

29/12/14

The patient was still quite ill and had frequent urges to defecate. He had frequent bouts of explosive diarrhoea and hyper flatulence. It was at 10pm that evening that the patient came under the care of a naturopath who had arrived from Australia and was staying at his residence. Upon first examination, the patient was delirious and complained of chills and shaking. Physical examination revealed upper abdominal tenderness, rigidity (guarding) and extensive bloating, but did not show Cullen's sign (umbilical bruising/oedema around the umbilicus) or Grey Turner's sign (bruising of the flanks) which could have been suggestive of retroperitoneal haemorrhage. The naturopath monitored the patient throughout the night having only intermittent sleep.

30/12/14

Upon waking the next morning, the patient felt that the original abdominal pain had slightly improved (5/10), but that the diarrhoea, intermittent nausea and excessive burping were still marked, along with transient griping pain from hyper flatulence (6/10). The patient had not eaten anything in several days at this point but was staying hydrated.

Navigating herbal selection in a foreign country is difficult. In this city (population: 60,000) there exists one major health food shop which is largely an organic produce store but did have nutritional and herbal supplements. This being said, the Food and Drug Administration (FDA) does not test the quality of ingredients of natural products in the US, making finding suitable products for dispensation difficult due to lack of standardisation or quality testing. Given that ethanol was likely causative in this case, no ethanolic tinctures or fluid extracts were used, but rather crude herbs in their natural form.

Treatment

Falling back on traditional foundations, the naturopath employed simple naturopathic philosophies for patient management. Firstly, obstacles to cure such as coffee, stimulants, purified sugar and excessive, large fatty meals were discouraged in favour of a highly nutritious and phytochemically dense diet. To establish conditions for health, which is in line with the first therapeutic order, a simple vegetable soup was made with butter, onions, garlic, carrots, celery, cauliflower, broccoli and zucchini and was finished with yellow lentils in filtered water. The base of the soup was rich (3 heaped tablespoons) in Curcuma longa (turmeric, dried powder) for its anti-inflammatory effects, with in-vivo evidence suggestive that in a rat model of experimental pancreatitis, curcumin reduced inflammation via inhibition of NF-kappa-B and activator protein-1. (9) Whilst turmeric can exert choleretic activity (10) and gallstones had not been ruled out, the practitioner still opted for the importance of a strong anti-inflammatory effect to assist the pancreas and also rectify gastrointestinal (GIT) hypermotility. Further supportive actions of turmeric, including hepatoprotective, hypolipidaemic, antioxidative (11) and carminative actions, were also desirable. This combined synergistically with the anti-inflammatory actions of Zingiber officinale (ginger, fresh rhizome x 1 heaped tablespoon) which also exhibits powerful antiemetic, carminative (12) and spasmolytic actions. (13) Allium sativum (garlic, fresh bulb x 3), like Zingiber officinale, was put in towards the end of cooking to preserve its volatile compounds and carminative, anti-inflammatory (14) and antimicrobial effects. Other crude herbs employed within the soup included aromatic digestives and carminatives in the form of Coriandrum sativum (coriander, fresh chopped leaf & grated roots x 1 bunch and dried powder x 2 tablespoons), Cuminum cyminum (cumin, powdered seeds x 1 tablespoon), Illicium verum (star anise, whole fruit x 3), Foeniculum vulgare (fennel, crushed seeds x 1 tablespoon), Ellettaria cardamomum (true cardamom, whole pods x 5) and a small amount of Piper nigrum (black pepper, ground fruit x 1/2 teaspoon). The soup was simmered gently for 2-3 hours until the lentils broke down, being stirred regularly.

At mid-afternoon, whilst the soup was being prepared, the patient consumed 2 tablespoons of Ulmus rubra (slippery elm, ground bark) mixed with enough water to form a drinkable solution, and followed by 2 glasses of water. This is in line with the third therapeutic order, supporting weakened or damaged organs, and the fifth order, addressing pathology using specific natural substances. (15) Ulmus rubra exerts demulcent and nutritive actions, with large amounts of mucilage soothing irritation of mucous membranes within the gastrointestinal tract. (14) This was followed 4 hours later with 2 heaped teaspoons of Plantago ovata (psyllium, dried husks) taken in a similar fashion but with less water in order to check the diarrhoea via its absorptive properties. (12) Both demulcent herbs were taken 2-3 hours away from any ingested medicines due to potential physicochemical interactions based on high mucilage content. (16)

Later that evening, the soup was salted to taste and served. Within an hour of having a small cup (250mL) of the soup, the patient reported considerable relief of upper abdominal pain (1/10 from 5/10) and complete resolution of the griping pain (0/10 from 6/10) caused by hyper flatulence. The pre-existing nausea was also completely resolved. The patient retired early and slept for 10 hours after one last half dose (1 tablespoon) of Ulmus rubra and water.

Upon waking the next morning, a very small portion of scrambled eggs with powdered turmeric was served. With colour and energy returning to the patient, a gentle, meandering hike in the local nature reserve was taken to stimulate the vital force and encourage ambulation, and thus fulfilling the second therapeutic order of stimulating the self-healing mechanisms (vis medicatrix naturae). (15) The hike was roughly 6km in length and 3 hours in duration, and the patient reported feeling tired but revitalized afterwards. He developed some loose stools later in the day and was treated again with Ulmus rubra bark. An infusion of Zingiber officinale radix (ginger, fresh rhizome) and Matricaria chamomilla flos (german chamomile, dried flowers) was also taken at this time pro re nata (PRN) for anti-inflammatory and spasmolytic activity, (17) with the patient's bowel movements normalising within 3 hours and continuing to be normalised throughout his convalescence. The following day the patient complained of symptoms suggestive of his non-specific prostatitis, but the remainder of his original symptomatology had ameliorated.

Follow up

Consulting with his regular general practitioner (GP) 4 days later, the patient was symptom free and was organising to see an urologist regarding his non-specific prostatitis. The GP did not feel that ultrasound or follow up investigations were needed to monitor the patient's pancreatitis based on his clinical presentation at this time.

Conclusion

There exists little evidence on potential naturopathic management strategies in the clinical and scientific literature for acute pancreatitis, which may largely be due to it being treated as a medical emergency. Nevertheless, when scientific or clinical evidence is lacking, one can rely upon traditional knowledge to support the patient's symptoms, deficient body systems and general health. The author wishes to make clear that in no way does this undermine the necessity for close medical supervision in such circumstances as disease progression can be potentially fulminant if infection, necrosis or other sequelae develop.

Of clinical interest, follow up research on the use of probiotics in acute (severe) pancreatitis has suggested an increased risk of mortality. (5,18) This is important to consider as many practitioners may consider prescribing probiotics in such a case due to it being beneficial to the gut. More research needs to be carried out in this area; however, until the underlying mechanism is revealed, prophylactic probiotics should be considered potentially unsafe. (5)

In conclusion, this case is a reminder that traditional naturopathic knowledge and philosophies still form a valid and useful source of evidence, and furthermore, how therapeutically valuable crude herbal medicines can be. This latter observation is easily forgotten and often overlooked in our current herbal profession, which is largely focused on commercially manufactured and standardised dosage forms.

References

(1.) Underwood JCE. Liver, biliary system and exocrine pancreas. In: Underwood JCE, Cross, SS, (eds). 2009. General & Systematic Pathology, 5 edition. London: Churchill Livingstone Elsevier.

(2.) Beers MH, Berkow, R. (eds). 1999. The Merck Manual of Diagnosis and Therapy, 17 edition. Whitehouse Station New York: Merck Research Laboratories.

(3.) Kumar P, Clark, M. (eds). 2005. Clinical Medicine, 6 edition. Edinburgh: Elsevier Saunders.

(4.) Frey CF, Zhou H, Harvey DJ, White RH. 2006. The incidence and case-fatality rates of acute biliary, alcoholic, and idiopathic pancreatitis in California, 1994-2001. Pancreas. 33(4):336-44.

(5.) Besselink MG, van Santvoort HC, Buskens E, Boermeester MA, van Goor H, Timmerman HM, et al. 2008. Probiotic prophylaxis in predicted severe acute pancreatitis: a randomised, double-blind, placebo-controlled trial. Lancet 371 (9613):651-9.

(6.) UK Guidelines for the management of acute pancreatitis. 2005. Gut 54 (Suppl 3):1111-1119.

(7.) Deitch EA. 1990. The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure. Archives of Surgery 125(3):403-4.

(8.) Ammori BJ, Leeder PC, King RF, Barclay GR, Martin IG, Larvin M, et al. 1999. Early increase in intestinal permeability in patients with severe acute pancreatitis: correlation with endotoxemia, organ failure, and mortality. Journal of gastrointestinal surgery 3(3):252-62.

(9.) Gukovsky I, Reyes CN, Vaquero EC, Gukovskaya AS, Pandol SJ. 2003. Curcumin ameliorates ethanol and nonethanol experimental pancreatitis. AM J PHYSIOL-GASTR L 284(1):G85-95.

(10.) Bone K. 2003. A Clinical Guide to Blending Liquid Herbs: Herbal Formulations for the Individual Patient. St. Louis: Churchill Livingstone.

(11.) European Scientific Cooperative on Phytotherapy Monographs. 2003, 2 edition. Stuttgart: Thieme Publishers.

(12.) British Herbal Pharmacopoeia. 1983. London: Scientific Committee of the BHMA British Herbal Medicine Association.

(13.) Bone K, & Mills, S. 2013. Principles and Practice of Phytotherapy, 2 edition. Sydney: Churchill Livingstone Elsevier.

(14.) Bradley P, editor. 1992. British Herbal Compendium. Dorset: British Herbal Medicine Association.

(15.) Zeff J, Snider P, Myers SP. 2006. A hierarchy of healing: the therapeutic order. In: Pizzorno J, Murray MT (eds). Textbook of Natural Medicine. 3rd ed. Missouri: Churchill Livingstone Elsevier.

(16.) Sinclair J, Sinclair, C. 2013. Polypharmacy and drug-nutraceutical interactions. In: Sarris J, Wardle, J, (eds). Clinical Naturopathy, 2 edition. Sydney: Churchill Livingstone Elsevier.

(17.) Braun L, Cohen M. 2007. Herbs & Natural Supplements: An Evidence-based Guide, 2 edition. Marrickville: Elsevier.

(18.) Besselink MG, van Santvoort HC, van der Heijden GJ, Buskens E, Gooszen HG. 2009. Dutch Acute Pancreatitis Study G. New randomized trial of probiotics in pancreatitis needed? Caution advised. Langenbeck's archives of surgery/Deutsche Gesellschaft fur Chirurgie 394(1):191-2; author reply 3-4.

Justin Sinclair (1,2)

(1) Traditional Medicine Consultancy, Pacific Pines, QLD Australia

(2) Endeavour College of Natural Health, 105 Scarborough Street, Southport QLD Australia

Email: j.sinclair@tmconsultancy.com.au
Table 1.1 Causes of Acute Pancreatitis (1-3)

Gallstones

Infections (Mumps, Coxsackie B virus)

Drugs (oestrogens, corticosteroids, azathioprine, furosemide,
valproic acid)

Iatrogenic (ERCP, post-surgical)

Abdominal trauma

Hyperlipidaemia

Pancreatic tumours

Hyperparathyroidism

Scorpion bite

Cardiac surgery

Idiopathic
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Author:Sinclair, Justin
Publication:Australian Journal of Herbal Medicine
Article Type:Report
Date:Jun 1, 2015
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