Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
The Complicated Patient – A Roadmap to Assessment and Therapy Dr. Paul Anderson Summary Being an integrative practitioner might make you the best trained and able to deal with the complicated patient but it sure can make your day long and complicated. In this final session Dr. Anderson will outline a process for assessing, quantifying and laying out a treatment plan for this challenging group of patients. The presentation will focus on top down assessment and categorizing therapies by the stage of the illness the patient is in (or “peeling the onion”). An appropriate thought process in which any appropriate modality can be inserted as well as a mechanism for reassessment will be outlined. Topic Summary Modern chronic illness is more complex and difficult to assess and treat than ever before. Aggravating factors such as infectious and immune effect, genomic variations, toxicants and others make the chronically ill patient complex. This session is designed to list the research behind these crossover points and to describe clinically relevant ways of untangling the clinical picture. Outline In this session Dr. Anderson will answer the questions: 1. My patients come in with so much going on; how do I know where to start? 2. They expect a quick fix of all complaints; how can I reset their expectation that this will take time? 3. What is the best way to make sure that we work together in alignment and how do I make them see they are making progress on a long road to healing? 4. Obviously this topic cannot be fully explored in one session or one day – but in addition to the above resources will be given for the practitioner to explore the topic more completely. Effectors in Chronic Illness Effectors: 1 7 1. Cell Function 2. Toxin 2 6 3. Biofilm 2 Sick 4. Immunology 5. Endocrine 6. Psychosocial 7. Digestive - GI 3 5 4 Note: Chronic Disease of any kind is (in the absence of genetic or acquired immune deficiency) is never a single issue. In some proportion the effectors listed feed into the terrain that allows the chronic illness to exist. How to think through the complex chronically ill persons case. Ideas - Concepts: Therapeutic integration and intensity: First Acute Illness LOW First / Early “clean” Chronic Illness MEDIUM Chronic Complicated Illness State HIGH Breadth and Depth of co-infection / co-morbidity etc Effectors in Chronic Illness Effectors: 1 7 1. Cell Function 2. Toxin 2 6 SICK 2 3. Biofilm 4. Immunology 5. Endocrine 6. Psychosocial 7. Digestive - GI 3 5 4 Note: Chronic Disease of any kind (in the absence of genetic or acquired immune deficiency) is never a single issue. In some proportion the effectors listed feed into the terrain that allows the chronic illness to exist. Effectors in Chronic Illness Effectors: 1. Cell Function 2. Toxin 1 7 2 SICK 2 3. Biofilm 4. Immunology 5. Endocrine 6. Psychosocial 7. Digestive - GI 3 6 5 4 Note: No person experiences these “layers” equally – and – they will change in proportion over time. So you must meet the case where it is and then monitor and adjust as the case evolves. Effectors in Chronic Illness Effectors: 7 1 1. Cell Function 2 2. Toxin 3. Biofilm 4. Immunology 6 SICK 2 5. Endocrine 6. Psychosocial 7. Digestive - GI 3 4 5 Note: In my experience as the case begins to clear up the residual effectors that take the longest can be these, although each person has their own “order” they heal in. Effectors in Chronic Illness Effectors: 1 1. Cell Function 2 2. Toxin 3. Biofilm 3 SICK 2 4 4. Immunology 5 5. Endocrine 6. Psychosocial 7. Digestive - GI 7 6 Note: All contributory factors must be consistently monitored even when they seem “normal” until the patient is healed – then a critical assessment of the initial inciting “weaknesses” must be done to focus prevention. Effectors in Chronic Illness Effectors: 1 1. Cell Function 2 2. Toxin 3. Biofilm 3 SICK 2 4 4. Immunology 5 5. Endocrine 6. Psychosocial 7. Digestive - GI 7 6 Note: In the preventive stage any area may be the weak point. All areas should be tonified and watched long term even in remission. So: Although we should not overcomplicate cases: We do need to take a step back in cases that are not clearing (or are getting worse) and recognize the effects our ever more toxic world, stronger infections, weaker immunity, biofilms etc have on the depth and breadth of our patients illnesses. Some Cases Slide Content (c) 2016 PS Anderson 14 Neuropsychiatric Case Slide Content (c) 2016 PS Anderson 15 Case - PT • 52 YO Female – Multiple psychiatric diagnoses that were resistant to multiple psychiatric medications over a 1 year trial. – Psychiatrists were frustrated and began adding medications without D/C of prior medications. – Patient presented with components of Bipolar I, Anxiety, and multiple other complaints. Case - PT • Patient agreed to getting a PICC line set, and an intensive course of IV treatment. • IV included two to three times weekly administration (in succession below) of: 1. IV – Phospholipids 2. IV Nutrients (Vit-Min- Amino Acids formula) 3. IV Glutathione Push at the end of Tx (1 – 4 grams) Case PT • Patient responded well acutely to the protocol. • She did better as we ramped the magnesium up in the Vit-Min AA protocol to a total of 4 grams magnesium sulfate per Tx. • Patient was instituted on oral nutrients between IV Tx: (PTC, Mg, 5HTP, B-Complex, Multi-Vit). – After 3 weeks we began a slow medication taper. Case - PT • We tapered the SSRI class of drugs first. – Patient responded well. • Patient eventually completed 40 Tx – 2-3X a week for 30 Tx – Then weekly for 4 Tx – Then bi-monthly for the balance of Tx. – Patient continues to this day (> 6 years later) on only oral nutrients and one low dose medication. Case: LK PANS – and other issues… Slide Content (c) 2016 PS Anderson 20 PANS PANS (Pediatric Acute-onset Neuropsychiatric Syndrome) is when an infectious trigger, environmental factors, and other possible triggers create a misdirected immune response results in inflammation on a child’s brain. In turn, the child quickly begins to exhibit life changing symptoms such as OCD, severe restrictive eating, anxiety, tics, personality changes, decline in math and handwriting abilities, sensory sensitivities, and more. PANS was introduced in 2012 by Dr. Susan Swedo in the paper From Research Subgroup to Clinical Syndrome: Modifying the PANDAS Criteria to Describe PANS (Pediatric Acute-onset Neuropsychiatric Syndrome). Case - LK • Patient: 18 year old male. • Date of first visit: August 2014 • Onset of illness: Early 2007 (following an acute illness) – Patient and mother report that he was “very normal” prior to the onset in 2007. • Primary presenting symptoms: – – – – – Fatigue Poor infection resistance Allodynia Circadian disturbance Increasing agoraphobia Prior Diagnosis and Treatment • From incident in 2007 through 2011: – Initially unknown trigger or illness – just sicker and sicker all the time – August 2011 a presumptive diagnosis: • “Unknown immune deficiency” • Therapy with IV-Ig – some help Prior Diagnosis and Treatment • 2011 New diagnosis: – After the above patient was diagnosed with elevated ASO and Positive titers – PANDAS / PANS • Treated with oral antibiotics, higher IV Ig doses • Patient flared so bad in late 2011 they were put on a slow Prednisone taper starting at 40mg. Prior Diagnosis and Treatment • 2011 New diagnosis: – With the therapy for the PANDAS / PANS (and as ASO/Cultures improved) • Less fatigue • MORE anxiety • Much MORE pain (“worst ever”) • Pain and Anxiety increase has the family on suicide watch. • Updates: then through our first visit: – Was currently on 1 mg Prednisone (taper from prior doctor – associated this dose with more symptoms). – Did try a biofilm nasal spray which seemed to help his symptoms Initial Assessment in August 2014 • Ongoing chronic illness since unknown trigger in 2007 • Prior Dx & Rx appeared to help some areas and not others – IV-Ig and some nutrient IV therapy helped most – Antibiotic therapies also seemed to modify the disease state • Need for: – Acute adjustment in the steroid Rx – New lab assessment required – Genomic assessment also required Initial Orders: • Order serum labs • Send me the genomic assessment • Increase the supportive IV Nutrient therapies – Increase nutrients slowly as indicated on SNP assessment – Attempt two IV per week separated by 1-2 days • Consider support to the IV therapies: – Based on the labs and SNP assessment possibly increased ID support, Biofilm therapies, HBOT etc. • Continue the basic nutrients and SQ-Ig injections Initial Report to Referring Providers • Background adrenal / steroid support: - Leave the 1 mg Prednisone for now, but to stabilize his system during this phase of the treatment we would add Hydrocortisone 10 mg in the AM (with the prednisone) and 10 mg at lunch. - This is well below the adrenal suppressive dose and will allow his system to more comfortably tolerate therapy. • IV: - Continue IV nutrients as before with steady escalation in doses as tolerated, and I will review all IV plans and orders prior to administration with each change. Initial Report to Referring Providers • IgG therapy: - Continue this as before • GcMAF: (Was a request of the parents that I comment on this) - As I looked over everything and listened to the history I believe this would be a positive addition for his immune function in the near future. I would recommend a Nagalase level be done as baseline soon (as this is a long lead time lab) and then that we consider GcMAF theray in the next month or two. I can supply dosing strategies should that be required. • Genomic Assessment: - Please see the addenda after this letter. - I am placing interpretation of the genomic areas of stress I see and their corresponding nutritional supports in that report. - I would think that adding them to the IV slowly over time and orally as tolerated would be the best plan. Additional Labs Ordered: • Confirmation of improved IgG levels (with infusions) • Confirmation of persistent IgA insufficiency • Confirmation of ongoing positive ASO and Anti-DNase B Strep Ab’s • Elevated Reverse T3 • Reactivated EBV (elevated EaIgG) and CMV at likely active titers (IgG at 10X elevation). • Negative ANA, HCYS at 11.2, CBC-CMP WNL, IgM and E normal Primary Genomic Assessment: • Phase-1 detox is relatively clear – There is one homozygous SNP at CYP2E1*1B G9896C rs2070676 • Metabolizes several precarcinogens, drugs, and solvents to reactive metabolites. Inactivates a number of drugs and xenobiotics and also bioactivates many xenobiotic substrates to their hepatotoxic or carcinogenic forms. This protein localizes to the endoplasmic reticulum and is induced by ethanol, the diabetic state, and starvation. The enzyme metabolizes both endogenous substrates, such as ethanol, acetone, and acetal, as well as exogenous substrates including benzene, carbon tetrachloride, ethylene glycol, and nitrosamines which are premutagens found in cigarette smoke. Due to its many substrates, this enzyme may be involved in such varied processes as gluconeogenesis, hepatic cirrhosis, diabetes, and cancer. Primary Genomic Assessment: • Phase-2 has some acetylation issues (NAT) as well as slow SOD activity. – This indicates a higher use of B-5 (for acetylation) – Also higher need for Trace minerals (especially Mn, Cu, Fe) Primary Genomic Assessment: • Plasma Cell activity: Generally reasonable but the one SNP in the IgG area found did have a homozygous defect. – This is likely part of the reason IgG therapy helps and should continue. – Homozygous - FCGR2A rs1801274 association with Kawasaki disease Duan J, Lou J, Zhang Q, Ke J, Qi Y, Shen N, et al. (2014) A Genetic Variant rs1801274 in FCGR2A as a Potential Risk Marker for Kawasaki Disease: A Case-Control Study and MetaAnalysis. PLoS ONE 9(8): e103329. doi:10.1371/journal.pone.0103329 Primary Genomic Assessment: • Other Immune: – Homozygous - IFIH1 (HLA) rs1990760 - IFIH1 Is Associated with Increased Sensitivity to IFN-α and Serologic Autoimmunity in Lupus Patients - J Immunol. 2011 Aug 1; 187(3): 1298–1303. – Homozygous - IL5 rs2069812 - Turk J Hematol 2014;31:17-24: The lack of other variants in the IL-5 gene of patients and controls suggests that rs2069812 may be a regulatory SNP and may have a role in B-lymphocyte development, constituting a genetic risk factor in antibody development. Primary Genomic Assessment: • Other Immune: – Homozygous - HLA rs2155219 - Associated with significant atopy - Hum Mol Genet. 2013 Dec 1; 22(23): 4841–4856. – Homozygous – SHMT2 rs34095989 - SHMT: Serine Hydroxy Methyltransferase (Helps to shift the emphasis of the methylation cycle toward the building blocks needed for new DNA synthesis and away from the processing of homocysteine to methionine.) Primary Genomic Assessment: • Methylation “family”: This group is generally experiencing a broad base of SNP activity in heterozygous formations. – This indicates that as opposed to a large effort to support one area (such as MTHFR) the better tolerated, and more helpful, path is broad based active B-Vitamin plus Trace Mineral co-factor support. Primary Genomic Assessment: • Retinoid conversion: He has 3 of 3 tested heterozygous BCMO SNP’s. – In the long run he will need retinal palmitate (fat soluble Vitamin A) at doses of 25,000 to 50,000 IU per week tapered to 5,000-10,000 IU for maintenance. This is because his Carotenoid to Retinoid conversion in globally hampered. This has potential effect on eye, gonad and epithelial tissue function. Primary Genomic Assessment: • Mitochondrial: If one looks at this area it is deceivingly “normal” but the homozygous NDUFS SNP’s as well as some others mean that conversion of B-3 to active NAD forms as well as efficiency of Co-Q-10 are hampered. – In the long run the Niacinamide in the IV B-Vitamins will help, and an NAD supplement with Co-Q-10 would be useful. Mitochondrial Support The role of mitochondrial dysfunction in disease: Damage to cell organelles (mitochondria, nucleus, ER, membrane) disrupts active transport, enzyme production and function & cell reproduction. These changes disrupt cell osmotic balance, transporters and other factors causing degenerative changes in the cell, tissue and eventually the person. Mitochondria: ELECTRON TRANSPORT / OX-PHOS – 1 • TCA cycle and Glycolysis only form a few ATP molecules each. • Most of the ATP from glucose metabolism comes from the electron transport system. • The main function of all the earlier steps is to make the Hydrogen of the Glucose molecule available in forms that can be utilized for oxidation. Mitochondria: ELECTRON TRANSPORT / OX-PHOS – 2 • Oxidation of Hydrogen is accomplished by Splitting the Hydrogen Atom into: – Hydrogen Ion – Electron • Electron used to change dissolved O2 from fluids to Hydroxyl ions. • Hydroxyl ions combine to form H2O • During these reactions, ATP produced. • Occurs in the Mitochondria • Occurs via Enzymatically Catalyzed Reactions Mitochondria: ELECTRON TRANSPORT / OX-PHOS – 3 SNP’s and Poisoning can disorder mitochondrial function: • Inhibition is Blocking the respiratory chain at places other than the ADP+P position. – Many poisons can do this: • • • • Barbiturates Rotenone (insecticide) Sulfuric Acid, CO, Cyanide Antibiotics: Oligomycin, Piericidin-A • Uncoupling (derailing) Ox-Phos: – Ox-Phos is the addition of ‘P’ to ADP = ATP – Uncoupling is the dissociation of oxidation from phosphorylation (Incr. permeability of mitochondria to protons / reduces electromechanical potential – short circuits ATP-synthase [ATPase]) • 2-4-dinitrophenol, dinitrocresol, pentachlorophenol Mitochondria: ELECTRON TRANSPORT / OX-PHOS SNP’s – 4 • The chemiosmotic mechanism of Oxidative Phosphorylation resulting in the formation of large amounts of ATP. • At the mitochondrial membrane. COX series NDUFS series UQCRC series ATP5 etc series Cofactors to consider: • • • • • • • Nicotinamide / NADH Co-Q-10 Riboflavin-5-phosphate Iron Proline Ca, Mg, K, Zn,Cu,Cr [positive] Cd [negative = mito poison] •Structure 19, 833–843, June 8, 2011 •African Journal of Food Science Vol. 4(5) pp. 200-222, May 2010 •J. Anim. Sci. Vol. 91, E-Suppl. 2/J. Dairy Sci. Vol. 96, E-Suppl. 1 Mitochondrial Damage • Big topic – Involved in the pathology of most chronically ill people • Slow to repair, but as it does the major symptoms lessen or are eliminated • Concepts are: – Clean up (curcumin) – Restore energy (LAMC [Poly-MVA], B-Vitamins, Iron [ferritin over 30-40 minimum], Thyroid - Adrenal, HBOT etc.) – Repair (Phospholipids, ALA, Carnitine, Taurine) – Attend to cell ReDox: Omegas / Tocopherols / Ascorbate / Glutathione Mitochondrial Damage • Can people tolerate those mitochondrial therapies all at once? • If not what does that look like? • What order should those therapies follow? Progression of Therapies • Began supportive / mito-tx IV therapies • Began trial of HBOT after the IV therapies • Began adrenal rebalancing therapy and steroid adjustment • Planned for IV Anti-infective treatments – Implemented in the first 60 days of therapy • Planned for biofilm treatments – Implemented in the first 60 days of therapy • Continued the SQ – Ig therapy Rx Progression 02-2015 through 082015 • IV Therapies: – Mito and Cell Support Formulas – Anti-infective and Immune Support Formulas – Biofilm augments • HBOT: – Trial at 45 min 1.3 + ATA – Increased time and O2 over time – Family purchased a chamber in 04-2015 – doing home HBOT 4-6 days a week • Additional palliative therapies: – Adjusted oral supps and meds as needed – Added GI support – Added and adjusted medical cannabinoid therapies Case Progression 02-2015 through 08-2015 • IV Therapies: – Adjusted the additives as tolerated and progressed doses through time – Increased the intensity of and frequency of the immune therapies • HBOT: – After initial trial doses the patient noticed a great deal of help in many areas of compliant (pain, sleep, energy…) – Worked up to 90 min Tx with cycling air breaks • Additional palliative therapies: – Worked with balancing CBD Rx and use of additional THC product later in the day – Gave patient instructions on home preparation of mixed constituent product A lot of “up and down” through early therapy: 02-2015 follow up notes: • URINARY: Bladder "shyness" worse. CBD helps and heat helps. • SLEEP: Was waking at 6am least week. Now 10:30-11am and going to bed around 11pm-midnight. Hard to fall back to sleep in am once he wakes. and sleeping 10-12 hours. • EENT: Ear sore and tested and it was yeast. Consistent running nose and mucus in thought- does not feel like he has a cold. Yellowish. • ENDO: Wakes feeling very cold and needs to take a bath. • GI: Oxy powder (Mg Oxide) for GI motility. • GI: Random nausea- a couple times past few month he felt like he was going to throw up for now reason may have been zinc on an empty stomach. Pressure build in stomach and he feel like he needs to burp it Burps up mucus. and he needs to swallow it down again. 02-2015 Plan: • • • • • • Adjusted Mito-Tx, IV formulas Added Thyroid and Adrenal support Increased GI support Added Xylitol nasal spray and saline Added consideration to use BEG spray Encouraged patient and family to stick with the plan. Family is frustrated but also sees some movement forward which is of some encouragement. 06-2015 Follow up: "Progress is slow but steady. Likely about 30% improvement from baseline" Biggest gains are in: - Energy - Social interaction - Functionality - Decreased neurological agitation - Less anxiety 06-2015 through 07-2016 • Some gains and some aggravations. Trend is better. • In 01-2016 changed ABX and added the oral Biofilm protocol with ‘Biosolve’ (see Biofilm notes). – After one month at full dose LK aggravated with a PANS flare. I met with he and his mother and we agreed this was breaking through a huge barrier to progression but also that we needed more gentle progress with the new biofilm therapy and new ABX. 06-2015 through 09-2016 • Over the 1.5 years the family and LK believe he is definitely moving toward better health and less PANS Sn/Sx. • There is still much to do and he does flare, but he has a life, and quality of life he has not had in years. Summary Slide Content (c) 2016 PS Anderson 56 Effectors in Chronic Illness Effectors: 1 7 1. Cell Function 2. Toxin 2 6 3. Biofilm 4. Immunology 5. Endocrine 6. Psychosocial 7. Digestive - GI Slide Content (c) 2016 PS Anderson 5 2 Sic k 4 3 Note: Chronic Disease of any kind is (in the absence of genetic or acquired immune deficiency) is never a single issue. In some proportion the effectors listed feed into the terrain that allows the chronic illness to exist. 57 Ideas - Concepts: Therapeutic integration and intensity: First Acute Illness LOW First / Early “clean” Chronic Illness MEDIUM Chronic Complicated Illness State HIGH Breadth and Depth of co-infection / co-morbidity etc Slide Content (c) 2016 PS Anderson 58 1. Meet and assess each patient where they are regardless of which disease label they have. As a cornerstone of being able to apply balanced and effective integrative care to patients the ability to assess their state of health and vitality while targeting treatment to their individual needs is paramount. The beauty of integrative medicine is that its many modalities have the most depth when incorporating into a complicated chronic illness care plan. In this the integrative plan can meet the person where they are and provide multimodality support. 2. Employ the most well rounded treatment, from any provider needed, and continue this through each phase of their care. After the above assessment, the application of integrative medicine and any other needed modalities can commence. Many times the practitioner has to stratify the modalities applied in a least to most important manner and decide what the patient needs and can realistically employ at their stage of health. In doing so the best support for the moment can be brought to bear on their case, and the likely “next steps” will be waiting in the wings for them as they progress or aggravate. 3. Regardless of where you have to start therapeutically always continually assess and treat the determinants of health. In the chronically ill person a conundrum often exists as to how many of the “basics” need to be or are implemented during an acute or severely chronic state. Examples might be “just how concerned with ______ should I be while I am so ill?” The blank can be diet, clean foods, exercise, mental emotional and spiritual practice etc. The answer is both fluid (based on the case and vitality of the patient) as well as dogmatic (the basic determinants of health are always important). 3. Regardless of where you have to start therapeutically always continually assess and treat the determinants of health. Rectifying this dissonance is key to appropriate clinical management. In reality the process is typically a discussion like this: “I realize you are in an acute state and feel horrible. I am going to discuss what we call your determinants of health so they are on your mind. What we will do is work toward these things being a larger and larger part of your care over time. And the reason for their importance is that eventually in order to keep you well these factors have to be consistently addressed – even if we are not doing a lot with them immediately.” 4. Embrace the seeming failures of treatment and “odd reactions”. I often tell patients that their body will process healing unlike anyone else, and their body has a language it speaks. The language is not verbal however, but rather presentation of signs and symptoms trying to tell us something. At this time I also tell them we learn more from what seemed to go wrong than what went right. 4. Embrace the seeming failures of treatment and “odd reactions”. Our goal is to not allow whatever went wrong to continue but rather let the body (and our knowledge of medicine) gain a new answer as to what to change or do next. I can personally say that the majority of things I know to do with very ill patients came not from medical school or educational offerings but rather listening to this language spoken by sick patient’s bodies and then finding the reason for and answer to that communication. 5. The progress of care is non-linear and so the therapies employed will necessarily be non-linear in their application. Just as we are going to meet the person where they are with their integrative care, we are also going to change the level and intensity of interventions as the person and their body process their specific healing path. This means communicating the need for follow up and reassessment with the patient, and being ready and able to adjust therapies. 5. The progress of care is non-linear and so the therapies employed will necessarily be non-linear in their application. Often as the higher force interventions complete their work there is a rapid need for more healing support. In this manner the patient is not told something like “everyone with your illness needs X weeks of Rx-1 then needs Y weeks of Rx-2…” If integrative medicine is given in too linear or formulaic a manner, it may over treat some areas while missing healing opportunities in the chronically ill patient. So • Give yourself and your patients time • Keep your mind open • Learn from success and learn more from failures • Get help if you need it Based on the principle of ‘Tolle Totum’ I am developing a multi-media program for advanced treatment skills. This will include live seminars, mentoring and web based programs for advanced chronic illness and cancer treating physicians. It elevates the ideas of truly integrative healthcare and modality integration which can effectively and successfully be used to all forms of chronic disease Oncologic, Immunologic, Infectious or whatever presents. Slide Content (c) 2016 PS Anderson 68 Thank you! Watch this site for webinars, documents, our new Fellowship Program and upcoming learning opportunities: WWW.ConsultDrA.com “Treat the Whole Person” Integrative Oncology & Chronic Illness Series: Advanced Applications in Medical Practice May 19-21 (Scottsdale, AZ) Slide Content (c) 2016 PS Anderson 69 Thanks and Be Well! Slide Content (c) 2016 PS Anderson 70