Emergency and Surgery Protocol for MCAS and ME

I started writing an emergency protocol back in 2015 when my mast cell reactions were scaring me with their unpredictability. I wanted something comprehensive, in writing, for anesthesia teams in the case of a planned surgery, but also something that my husband could hand to paramedics or emergency room doctors, if I couldn’t speak for myself. It was a massive undertaking because I tracked down every link and reference I could find about medication and surgery precautions for patients with mast cell diseases and ME. I wanted to gather all the information that was pertinent to me — my particular case — and edit it down to something manageable. I put together something passable and then moved it to the back burner for the last 4 years.

Last week I saw a new GI doctor who was emphatic that I get a colonoscopy and endoscopy at the same time and with anesthesia. I have been completely enema-dependent for years and, honestly, it’s exhausting. My previous GI doctor told me it was due to anatomical abnormalities (an MRI found pelvic floor dysfunction with cystocele, rectocele, sigmoidocele) and that I’d likely need enemas for the rest of my life, but it feels like the issues are getting worse and the new doctor didn’t want to throw medications at the problem without knowing exactly what she’s dealing with.

I cannot imagine voluntarily going under anesthesia. All of my worst reactions in the past 7 years have been to medications and my fear of trying new ones — especially intravenous medications — is so pronounced that I vowed only to agree to anesthesia if I was in a life-threatening situation (or couldn’t speak for myself). How could I be lying on a gurney with a peripheral IV, knowing they are about to inject multiple anesthetic drugs and not jump up and run out of the room? I wouldn’t be able to advocate for myself… I could die for a colonoscopy! So, I left the appointment with a sense of doom that only deepened when I started to feel a new ache in my lower abdomen. It got progressively worse over 3 days, the ache turned to pain and, what I thought of as run-of-the-mill bowel inflammation started to seem like something else. Gallstones? Bladder infection? I got out my emergency protocol notes and spent about 20 hours over the next few days rewriting everything, feeling like I might be working against the clock if this was something like appendicitis. Then I woke up last Sunday to such severe lower abdominal pain that I couldn’t move, could barely breathe or speak. I was shaking all over, in a cold sweat, nauseous and felt like I was on the brink of passing out. My husband wanted to call an ambulance, but I said no, hoping it was some sort of spasm that would pass. And it did… but not entirely. The ache and twinging remained for a few more days. It’s gone now and I think it was my dastardly bowels, after all, but it was bad and it scared me. It’s like the gods heard me say, “no way am I getting a colonoscopy” and decided to stab and twist their Elizabeth voodoo doll to make sure I got the point that there’s a problem I can’t continue to ignore.

The upshot of all this is, I finished the emergency protocol and I wanted to share it here, in case it could be useful to anyone else. There are a few important points about it, though:

  1. When I started, it was for personal use and I didn’t keep track of references. I will go back and gather all the links and add them to this article, but I have no idea how long it will take me and I wanted to share this sooner, rather than later. If you see your own information here without credit, please understand I will add a link to your article/blog/website! If you want me to do it asap, feel free to leave a comment.
  2. This protocol concentrates heavily on mast cell precautions because MCAS has caused my life-threatening reactions such as anaphylaxis and profound hypotension. It does not mention ME or CFS, although I researched and included ME resources, such as Dr. Lapp’s recommendations (Appendix E of the Primer for Clinical Practicioners).
  3. I have an EDS diagnosis (Ehlers-Danlos Syndrome — a connective tissue disorder), which can cause serious surgical complications. There are a lot of guidelines out there for EDS patients and, as yet, I have not researched any of them. It wasn’t until recently that I started to take this diagnosis more seriously and I still haven’t had the gumption to jump down the research rabbit hole, but, once I do, I will be updating my surgery protocol with any additional EDS precautions that are pertinent to my situation.
  4. It bears repeating: This is not medical advice of any kind. This is my personal protocol, for my personal situation. You may be more or less reactive than I am, you may have normal or high blood pressure or you may be far more disabled and need many more accommodations… But, I hope it can be of use as a jumping-off point. Please consult with your doctor.
  5. The link below is a printable pdf file, which is formatted properly, but I also wrote the protocol in its entirety on this page so others could copy and paste anything they wanted into their own protocols.

Elizabeth Milo Emergency and Surgery Protocol


The most important considerations in emergency situations and for surgery are:

  • My reactivity and hyper-sensitivity to medications, which necessitates very low dose and slow administration (see attached allergy listI have reacted to Morphine and Morphine derivatives with breathing difficulties).
  • I HAVE NEVER HAD ANESTHESIA and cannot predict how I will respond to medications.
  • Maintaining my very low blood pressure.
  • My history of idiopathic and atypical anaphylaxis with syncope.
  • Avoiding vasodilators and histamine-releasing agents.
  • I have cervical spine instability and care must be taken not to damage or hyperextend my neck.

For a patient with mast cell disease, the stress of surgery is compounded by the possibility of complications such as anaphylaxis, cardiovascular collapse, increased bleeding and even death. Therefore, general anesthesia is considered a high-risk procedure in patients with mast cell disease. It is critical that all members of the patient’s operating team take proper precautions before, during, and after surgery to protect against potentially life-threatening mast cell reactions.

An experienced anesthesiologist is aware of medications known to cause mast cell degranulation and medications that stabilize mast cells. If the patient is satisfied that their anesthesiologist fully understands the importance of planning around mast cell disease, it will go a long way toward calming the patient, which in turn may reduce mast cell mediator release. Bear in mind that some of the most common mast cell triggers are medications, pain, stress, hormones, temperature extremes, molds, perfumes, cleaning products and detergents.


Review medication and supplement list with the surgical team. I will stop as many medications and supplements as possible at least a week in advance, especially ones that lower blood pressure (vasodilators such as aspirin, nitroglycerin, vitamin E).

Discuss premedications. Some procedures require the patient not to take anything by mouth including medications after midnight the night before surgery. In this case, discuss administering H1- and H2-blockers intravenously prior to the surgery (note: I have never had IV antihistamines, so this is a concern). Premedication with corticosteroids may also be indicated. Ask anesthesia team and surgeon if I am allowed to drink clear fluids before surgery and be sure to be adequately hydrated.

Discuss medications that will be used during surgery. I have mast cell activation syndrome and a history of idiopathic anaphylaxis. Anaphylactic episodes are generally treated with intravenous H1- and H2-blockers and IM epinephrine, if there is hemodynamic instability or respiratory distress. In addition, IV fluids and other support and resuscitation measures should be undertaken.

I am unusually reactive to small amounts of medications. All medications should only be used if absolutely necessary and then used sparingly and in small doses until my response can be assessed. For example, I have had reactions to every benzodiazepine I’ve tried (tongue swelling, respiratory distress, migraine) and am very sensitive to even antihistamines. I have autonomic nervous system dysfunction. Due to this, anesthetics can cause gastro-esophageal reflux, tachyarrhythmias and difficulty maintaining blood pressure. It may be prudent to perform a graded challenge procedure in the hospital under the supervision of an allergist and an anesthesiologist for certain medications if there is no history of exposure to that medication. This procedure usually starts with scratching the skin with a small amount of medication followed by injection of increasing amounts with careful monitoring after each injection. 

I have very low blood pressure and probable depleted blood volume. Intraoperative hypotension is one of the most encountered factors associated with death related to anesthesia. Consider an intra-arterial catheter for continuous blood pressure monitoring during surgery (as opposed to a cuff). Discuss how hypotension will be treated during surgery (print study).

Controlling the depth of anesthesia limits the hypotensive effect of anesthetic drugs. Deep hypnosis (BIS <45) has been associated with postoperative complications and mortality. To limit hypotension induced by intravenous drugs, anesthesia should be titrated to clinical response. To guide induction anesthesia and identify the depth of anesthesia, consider bispectral index (BIS) monitoring.

Discuss continuous IV hydration to maintain blood pressure, however, please note that I have had reactions to IV fluids in the past due to running them too quickly or the saline being too cold. I typically run 1 liter of B. Braun Excel normal saline over a maximum of 4 hours. Fluids should be warmed in a 35-40 degree celsius water bath.

Discuss pain control: I have had reactions to Morphine and its derivatives and NSAIDS.

I have low cortisol and take daily low-dose hydrocortisone. Consider a 24-hour urine free cortisol level before and after surgery. A liver panel and serum cortisol should also be checked prior to any general anesthesia. I will double or triple my hydrocortisone dose before and after surgery.

Check serum electrolytes, in particular red blood cell magnesium (an intracellular test) and serum potassium and replenish if borderline or low. Low magnesium or potassium depletion could potentially lead to cardiac arrhythmias under anesthesia. Consider potassium 10 mEq, 1 tablet BID, and magnesium sulphate 50% solution, 2cc. IM 24 hours prior to surgery.

I have sleep apnea and asthma. Discuss the use of oxygen throughout procedure (use a disposable mask, not a reusable one in case of sensitivity to disinfectants). A preoperative lung vital capacity could be helpful. (The marker for real difficulty is thought to be a VC <1.0 liter. Such a patient needs good pulmonary preparation before surgery and a plan for postoperative ventilatory support.)

Discuss possible airway difficulties (review C-spine flexion-extension MRIs, if needed), such as: neck pain, cervical spine subluxation, limitation of cervical spine movement, nerve root impingement and/or spinal cord compression. I have a diagnosis of Ehlers-Danlos syndrome (EDS), TMJ disorder, cervical spinal stenosis, degenerative disc disease in my cervical spine and a previous neck injury. Care must be taken to keep my head and neck in a neutral position during surgery. Discuss wearing a soft neck collar to reduce neck hyperextension; this might help minimize inadvertent stretching of my neck muscles during intubation or use of an endoscope. To avoid neurological damage, patients with cervical spine instability should generally be intubated and positioned awake before surgery. This can also help assess the possibility of arytenoid involvement and determine the size of the glottic opening. The TMJs must be examined to ensure that mouth opening and anterior subluxation of the mandible will permit direct laryngoscopy/intubation. Also, be aware that the larynx may be displaced from its usual location by erosion and generalized collapse of the cervical vertebrae.

Pressure dressings are indicated even for minor procedures because excessive bleeding is common in mast cell disorders, even when blood counts are normal (this is related in part to the release of heparin during mast cell degranulation). For major procedures, a history of mast cell disorder should be included in bleeding risk assessment and may require special protocols. (I have included this in During Surgery discussion, also.)

The surgical team should be aware that I should not be exposed to perfume or scents at any time before, during or after the procedure.

Discuss post-operative recovery accommodations in the hospital, if needed — see After Surgery section. 


Constant attention from the anesthesiologist is required for the safety of a patient with mast cell disease, as some symptoms of mast cell mediator release such as flushing, hives, and early signs of obstructed breathing can be masked by surgical drapes and airway tubes.

Prior to the administration of any drugs associated with surgery, it is important that an IV is running, epinephrine is available for immediate intramuscular (IM) or IV administration, and emergency resuscitation equipment is easily accessible in case of an adverse reaction.

Be sure the patient does not become either too cold or overheated. I have subnormal body temperature (typically ~97.7). Warm blankets should be used and all IV fluids should be warmed (not over 40 degrees Celsius) before they are given. In addition, there should be a minimum of noise and bustle prior to the administration of the anesthetic in order to reduce the possibility of anxiety-triggered mast cell mediator release.

Intravenous (IV) fluids should be continuously running to keep the patient well-hydrated in all surgeries involving general anesthesia or conscious sedation. Hypovolemia resulting from blood loss or dehydration is a frequent cause of hypotension in the perioperative setting. IV access will also make it possible to immediately administer any emergency medications that may be needed. Hypotension episodes should be promptly treated by intravenous vasopressors — and/or antihistamines/epinephrine, in the case of anaphylaxis. 

Although the diagnosis of anaphylaxis usually depends on the involvement of 2 organ systems, even if it presents with 1 organ system, such as the skin, epinephrine administration may be indicated. Anaphylaxis may present as an acute cardiac or respiratory event, with hypotension as the only manifestation. Should anaphylaxis occur during surgery, the drug thought to be responsible should be discontinued immediately and rescue medications should be administered (H1 and H2 antihistamines, corticosteroids, airway support with 100% oxygen, IV replacement fluids to compensate for dilated blood vessels, bronchodilators). Because of the risk of potentially lethal arrhythmias, IV epinephrine should only be administered in profoundly hypotensive patients or patients in cardio/respiratory arrest who have failed to respond to IV volume replacement and several IM doses of epinephrine. *I am extremely sensitive to epinephrine, so even IM epinephrine should only be used if completely necessary. I am also extremely sensitive to antihistamines, so care must be taken to use the lowest dose possible and push very slowly. Vigilantly monitor me for reactions to rescue medications, also.*

*See anaphylaxis protocol below*

It is important to keep in mind that not all hypotensive episodes during surgery are due to mast cell degranulation/anaphylaxis. It would be ideal to get blood tests during a reaction, especially tryptase (see recommended tests below).

One of the most important considerations during anesthesia is maintaining a neutral neck position. A hyperextended neck can increase spinal cord compression and this, coupled with hypotension, which decreases blood flow to the spinal cord, can have a severe effect. Due to EDS and osteoporosis, my head, neck, pelvis and limbs should be moved carefully (limbs kept close to my body). 

Excessive bleeding is common in mast cell disorders, even when blood counts are normal. Pressure dressings are indicated even for minor procedures.


If the patient is being admitted to the hospital, discuss what is needed for a safe recovery:

  • Request a private room or a sound-proof door (versus an open curtain) and placement on a quiet ward.
  • Explain any sound, light, or chemical/fragrance sensitivities and the need for scent-free nurses (a sign next to the patient’s door can help remind nurses changing shifts).
  • Discuss any food sensitivities.
  • Discuss temperature sensitivities and the need for extra blankets or adjustment of the thermostat.
  • Ask whether it’s possible to minimize nighttime disruptions (for example, middle of the night blood pressure monitoring).
  • Discuss the potential need for extra recovery time in hospital or for a reclining wheelchair or gurney during discharge from the hospital.
  • Bring your own soap, hand sanitizer and bedding.



Consider using (but administer with extreme caution):

  • Diprivan (propofol) as the induction agent. (However, Propofol, used alone at induction of anesthesia, promotes a significant decrease in arterial blood pressure compared with thiopentone or etomidate, even with reduced doses.)
  • Versed (midazolam)
  • Fentanyl (a short-acting narcotic; may require adjunct treatment with Zofran)
  • Droperidol (an anti-nausea agent)
  • Tylenol
  • Tramadol

Second choice is ketamine or benzodiazepines, such as midazolam (however, I have had reactions to benzos in the past).

Atarax (Hydroxyzine) should only be used in an emergency. It can cause heart palpitations and arrhythmias. Doxepin should only be used at very low doses (<5mg — I have never taken it).

A small amount of Diazamuls, a preservative-free Valium emulsion, could be considered for long surgeries where the possibility of “awareness” is a concern. This drug can also be used pre- and post-operatively for sedation, and for cramping in certain types of procedures.

Use IV preparations without preservatives or alcohol. Use B. Braun Excel normal saline. Do not use lactated ringers, if possible.

Oxygen should be used throughout procedure (possibly at 5 liters pre and post-operatively). 

Do not use epinephrine except in life-saving situation. But Epinephrine must be on hand during the procedure.

Do not use medications that contain preservatives, artificial colorings, dyes, flavorings or alcohol (topical alcohol, as in alcohol prep pads, is fine, as is povidone iodine). Single-use vials are usually preservative-free. 

Do not use medications that stimulate neurogenic syncope or lower blood pressure: 

  • No cathecholamines (Epinephrine)
  • No sympathomimetics (Isoproterenol)
  • No vasodilators (nitric oxide, nitroglycerin, alpha-blockers, and hypotensive agents)

I have orthostatic hypotension (OI), chronically low blood pressure and a history of vasovagal syncope. Many people with dysautonomia have low plasma volumes, low RBC mass, and venous pooling and the above drugs may cause or exacerbate these conditions. 

Do not use histamine-releasing anesthetic agents:

  • No Sodium Pentothal or other thiobarbituates (Thiamylal, Thiobarbital etc.)

Do not use histamine-releasing muscle relaxants:

  • No muscle relaxants in the Curare family, such as Tracrium and Mevacurium.
  • No Succinylcholine ((Anectine) often causes severe, generalized muscle pain, post-op.)
  • No D-tubocurarine
  • No Metocurine
  • No Doxacurium
  • No Atracurium
  • No Mivacurium
  • No Rocuronium

Muscle relaxants are the most likely group of the anesthetic drugs to cause anaphylaxis. If muscle relaxants must be used, the current recommendation is to start with a quarter to half the usual dose of whatever you’re using. Intraoperative neuromuscular monitoring helps prevent overdose. Consider using “nondepolarizing” muscle relaxants, such as pancuronium or vercuronium. 

Do not use anesthetic gasses:

  • No Halothane
  • No Enflurane
  • No Isoflurane
  • No Desflurane

These can cause problems for patients with chemical sensitivities and are highly hepatoxic. An alternative might be continuous IV infusion of a short acting anesthetic by injection or a continuous flow pump. If necessary, consider Sevoflurane.

Do not use:

  • No Morphine, codeine or morphine derivatives
  • No Opioids
  • No Vancomycin
  • No Ethanol
  • No Dextran
  • No Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and Toradol
  • No Polymyxin B
  • No Amphoteracin B
  • No Quinine
  • No Dextromethorphan
  • No Alpha-adrenergic blockers
  • No Beta-adrenergic blockers
  • No Anticholinergic drugs, if possible, such as Hydroxyzine and Cimetidine
  • No decongestants, cold or flu medications
  • No SSRIs

Do not use local anesthetics, if possible. If needed, do not use ones with preservatives or epinephrine:

  • No Procaine
  • No Chloroprocaine
  • No Tetracaine
  • No Benzocaine

Consider using:

  • Lidocaine
  • Mepivacaine
  • Prilocaine
  • Bupivacaine
  • Levobupivacaine
  • Ropivacaine

Antibiotics are not well tolerated by mast cell patients, however, these are some that have been reported as safest by patients (use with caution):

  • Clindamycin
  • Cephamandole
  • Azithromycin (Z-pak)/Zithromycin/Zithromax
  • Keflex
  • Omnicef
  • Beconase AQ
  • Biaxin (eg. Clarithromycin)
  • Rhinocort


MEDICAL EMERGENCY RESPONSE PLAN for Mast Cell Activation and Anaphylaxis:

If the patient presents with flushing, rash, hives, swelling, abdominal pain, nausea, vomiting, shortness of breath, wheezing or hypotension, respond with the following: 


  • Epinephrine (preservative-free) 0.3 cc of 1:1000 (1mg/1ml) solution = 0.2mg–0.3mg IM (Vastus Lateralis muscle) and repeat 3x at 5–15 minute intervals if BP < 90 systolic (my BP averages 86/55).
  • Benadryl (diphenhydramine) 25mg (max 50mg) orally, IM or very slow IV push, diluted in normal saline over 2-5 minutes. Can repeat every 2–4 hours.
  • Solu-Medrol (methylprednisolone) 120mg (40mg for children under 12) IV/IM (I have never had Solumedrol, so monitor closely. My usual steroid is oral Prednisone 6mg)
  • H2 antagonist, such as Famotidine IV, should also be given (I have never had this, either — my usual H2 blocker is oral Zantac 150mg). 
  • Oxygen 100% by mask or nasal canula.
  • Albuterol nebulizatio,n if wheezing present.
  • IV fluids (warmed in 35–40 degree celsius bath and run as slowly as possible for the situation).

*All mast cell patients must be monitored for biphasic (rebound) reactions.*

Pre-medication for major and minor procedures:

  • Prednisone 50mg orally 24 hours and 1–2 hours prior to surgery (I’ve never had more than 7mg)
  • Benadryl (diphenhydramine) 25–50mg orally, 1 hour prior to surgery
  • Zantac (ranitidine) 150mg orally, 1 hour prior to surgery
  • Singulair (montelukast) 10mg orally (5mg for children under 12), 1 hour prior to surgery (I’ve never had Singulair)

*Note: my current premedication protocol is 25mg oral diphenhydramine (Benadryl brand dye-free capsules only), 150mg oral ranitidine (Zantac brand), 6mg oral Prednisone and 325mg acetaminophen (Tylenol brand).**

Drugs to be avoided:

  • Aspirin and non-steroidal anti-inflammatory (NSAIDS) medications
  • Morphine, codeine derivatives
  • Vancomycin



  1. Serum Tryptase — upon arrival in the ER and three hours later.
  2. 24 hour urines for:
    1. n-methyl histamine
    2. prostaglandin D2 ( PGD2)
    3. 11-beta prostaglandin F2 alpha (BPG-F2A)
  3. CMP
  4. CBC with differential

Also consider:

  1. Chilled plasma histamine
  2. Chilled plasma prostaglandin D2 (PGD2)
  3. Chilled plasma heparin
  4. Serum chromogranin A
  5. Serum magnesium

If possible, hourly determinations of serum tryptase, plasma PGD2 and histamine, and spot urinary PGD2 and N-methylhistamine should be pursued at baseline and over the next 2–3 hours as a reaction evolves.


The short half-lives and thermolability of many mast cell (MC) mediators require continuous specimen chilling throughout collection, storage, and transport. Particularly with regard to 24-h urine collections for MC mediator testing, patients should be carefully educated to pre-chill the collection container overnight before beginning the collection and then to keep the container continuously chilled while following an otherwise standard 24-h urine collection protocol; the container should be removed from the refrigerator or ice chest only when imminently needed and should be returned to chilling as soon as possible. Patients should also be cautioned to maintain the container in a chilled environment throughout transport. We recommend the container be placed in a bag filled with ice and sealed, with the bag then placed in an ice chest filled with ice and sealed for transport to the accessioning lab, whereupon the bag can be removed from the chest and provided to the technician with a reminder of the criticality of keeping the specimen chilled. Laboratory staff often are unfamiliar with MC mediator testing, previously a rarely undertaken endeavor. Consideration should be given by the diagnostician to sharing with laboratory personnel the ultimate clinical goal of such testing and the importance of maintaining thermal integrity of these specimens at all times, including at the time of initial accessioning as well as when packing specimens for transport to reference laboratories that may be thousands of miles distant, transits that may involve long periods sitting in unventilated cargo containers on hot tarmacs. Use of well-insulated containers, and liberal placement of cold packs in the insulated container, should be de rigueur when packing such specimens for long-distance transport.


You MUST have your allergist or primary care provider sign the bottom of this form stating that

he or she will be responsible for the follow-up on the 24 hour urine collections. Otherwise, the ER physicians will be reluctant to order them since they cannot be sure of follow-up care. Remember to contact your physician for follow-up after discharge.


I agree to provide follow-up care for my patient,____________________________________, and will obtain the results of the 24-hour urine collections that were initiated in the emergency room setting and will provide appropriate care based on the results.


Printed Name of Physician


Signature of Physician Date

Contact Address_________________________________________


Phone Number__________________________________________

Fax Number_____________________________________________



Acute coronary syndromes can occur in allergic and anaphylactic reactions. One example, called Kounis Syndrome, is highly likely in patients with a wide variety of mast cell activation disorders and can affect patients of any age. The main triggers of Kounis syndrome are drugs, environmental exposures, and various pre-existing conditions. When patients are on a protocol exposing them to many medications, the cascade leading to anaphylaxis and Kounis syndrome can be very rapid, with the heart and coronary arteries as the primary target. Multiple mast cell mediators have direct action on coronary vessels and together result in hyperresponsiveness of mast cells, which can result in the Kounis syndrome cascade. Please note: Coronary artery spasm induced by mast cell mediators may initiate Takotsubo Syndrome or stress-induced cardiomyopathy during anaphylactic reactions.

Type 1: Normal coronary arteries, no coronary disease, no predisposing conditions; acute allergic attacks resulting in coronary vasospasms without elevations in cardiac enzymes OR coronary vasospasm with myocardial infarction with elevation of cardiac enzymes and troponins.

Treatment of the allergic episode can terminate the type 1 variant

  • Corticosteroids
  • H1 and H2 blockers
  • Vasodilators such as calcium channel blockers and nitrates can decrease hypersensitivity induced vasospasms

Type 2: Quiescent pre-existing atheromatous disease in whom acute allergic attacks can induce either vasospastic angina or plaque erosion, or rupture manifesting acute myocardial infarction.

Treatment of acute coronary event comes first, then treat allergic attack:

  • acute coronary event protocol
  • Corticosteroids
  • H1 and H2 blockers

Type 3: Stent thrombosis with eosinophils and mast cells identified on pathology (Giemsa, hematoxylin-eosin stain).

Treatment of stent thrombosis with allergic attack:

  • Corticosteroids
  • H1 and H2 blockers
  • Mast cell stabilizers
  • Biopsy of thrombus stained for mast cells and eosinophils. Nitroglycerin causes decreased blood pressure and increased heart rate. 

Fentanyl is the opiate with the best profile for mast cell patients; administer with extreme caution.



Nonimmunologic Histamine Releasers and Other Degranulation Triggers

Foods and misc Chemicals & Drugs Physical Agents
Compound 48/80
Calcium ionophore A23187
Bacterial Toxins
Snake venoms
Biologic polypeptides
Ascaris species
Portuguese man-of-war
Spines & hairs of Caterpillars
MothsFoods high in Histamine or Tyramine, Gluten, Soy, Salicylates (eg: fish, strawberries, egg whites, tomato)
Foods containing preservatives, artificial colorings or flavorings.
Opiates (Codeine, Morphine, Percocet, Oxy etc)
NSAIDs (Advil, Motrin etc)
Polymyxin B sulfate
Colistin sulfate
Thiamine hydrochloride
Trimethaphan and Trimetaphan
Tubocurarine chloride
Quinine sulfate
Dipyridamole (Persantine)
Iodine-based radiographic dyes
Scopolamine hydrochloride
Neuromuscular blocking agents (eg: Dexamethonium, Gallamine triethiodide etc)
Dextromethorphan (cough suppressant)
Stilbamadine isethionate
Chlortetracycline bisulfate
Hydralazine hydrochloride
Tolazoline hydrochloride
Cinnamic acid
Benzoic acid
Sodium benzoate
Fungal infection drugs
Local anesthetics: lidocaine etc. (any amino amide-type)
Dermatographia (Darier’s Sign)
Hot baths/showers
Occlusive dressings
Eating spicy foods
Emotional stress
Solar light waves
Insect bites (Wasp, Hornet, Bee, Mosquito)
Smoke (wood burning, cigarette, marijuana) Scents/Odors/Perfume
Cleaning products and chemicals
Cosmetics/Creams containing salicylates
Preservatives, Additives, Dyes, Artificial flavours/colouring
Internal diseases


Screenshot 2019-07-13 at 11.45.21 PM


More IVIG reactions

I had to abort my last IVIG infusion because I had a reaction to my IV fluids and then, once I started the gammaglobulins, developed chest/throat hives almost immediately. That was always my anaphylaxis red flag in the past and, like I said last month when I got that hive on my throat at the end of my infusion, I haven’t had this happen in 17 years. I don’t want to go back to those days, so I’ve spent this weekend with a sense of doom and fear. Anaphylaxis scares me more than anything else.

I only got 1 gram of IgG into me and had to throw out the rest: $1,024 worth of medication down the drain ($205 of my own money). I’m going to try again on Wednesday, though. This treatment is too important. Even the IV fluids without the medication are too important to lose. And I want to have that protective boost for our upcoming road trip to California to see my specialist, Dr. K. It scares me to try again so soon after a reaction, but I’ll double my steroids and maybe my antihistamines, too. Please let me have this win, universe. 🙏

Also today, I gave up on the 30-day heart rate monitor after only 10 days. When I peeled the sticky electrodes off, my skin went with them. Bad, painful rash. (Note: this photo is actually from the 48-hour HR monitor not the 30-day one–the skin wasn’t actually broken here, just red–but I can’t take a photo today because I’ve slathered the rashes in calendula).

It’s frustrating because a) I don’t usually react to adhesives and b) I’ve already been a pain in the ass to this clinic by having to return the first set of wires because they STANK of the last person’s perfume (people: perfumes never come out of porous material! They’re a NIGHTMARE) and then I had to return the second set of wires because they were brand new and the manufacturing-chemical-rubber-hell-smell was even worse than the perfume! I had a full-on flushing event having those connected to my chest.

So, two more healthcare fails this week. On the plus side, I am tolerating Xifaxan, Lovastatin and Interphase, three new medications for my gut/bowel problems, with no side effects. Go figure.

The future might be the past…

I’m going through a rough(er) patch. My body is scaring me because I can’t find any cause for recent episodes. One of the good things these past few years, is that I can usually pinpoint a reason for reactions and downturns. Even after the last horrific night I suffered with apparently no reason (it was last November, during my Dad’s very short visit and I couldn’t blame it on overdoing it because I didn’t), I started spotting late the next day and–light bulb!–it was my period coming a week early (I can have terrible reactions on the day before or the first day of menstruation).

When my husband called 911 on the first day of my last period (both my MD and ND said that my body had gone into shock), it was the first time I’d had such a bad collapse with vitals bottoming out since 2010 — since before I was sick! Then, 5 days later, I got a tingly tongue and lip during IVIG and then a hive on the base of my throat. I realise it was a tiny reaction compared to what so many mast cell patients go through (a week later, a friend of mine went into full-blown anaphylaxis during her IVIG infusion and then somehow got the guts to try again the next day with the same batch –that put my experience into perspective), but the thing is, except for one small hive when I tried Xanax in 2013, I hadn’t had any hives since being in full-blown anaphylaxis 17 years ago! And that place–a hive in the suprasternal notch– was always the position for a systemic red alert, for something I ingested, as opposed to benign contact dermatitis.


Then Saturday evening, my tongue swelled up for the first time in 7 months for no reason that I can figure out. I had tongue swelling a few times last year, but I could always explain it (dental work, sauna, vancomycin). Even more concerning, it’s still swollen now, 45 hours later and that’s very unusual. I took Benadryl the last 2 nights, squirting it onto the affected area of my tongue, as I’ve been told to do (this is also unusual for me–I am extremely judicious with Benadryl, only taking it when absolutely necessary) and the swelling still hasn’t resolved. I can’t remember another time it lasted this long — maybe, again, 17 years ago during anaphylaxis.

Then yesterday afternoon, I was hit with vertigo after spending too much time on my feet, preparing food. Vertigo is rare for me and is a big red flag. It’s very different from dizziness and I don’t think it has anything to do with blood pressure. I went to bed for a while, hoping it would resolve, but, when I got up, I was still slamming into walls, as if I were walking the hallway on a lurching boat. The last 2 times I experienced vertigo were 5 months ago during–shocker–my period and a year ago on the morning we were leaving for California, after killing myself the day before to finish packing. I thought it might be something to do with my neck, which always has issues, so I used heat, then my cervical traction device, then an ice pack. I think it helped; the vertigo had mostly abated by the time I went to bed.


A few hours after I went to sleep, I woke up with horrible shakes and chills and drenching sweats. My BP was low (but low-normal for me: 80/50), HR was a little high, temperature was 96 degrees, and O2 was 95%. It was 7 terrible hours that felt viral, like when I first got sick, but was probably mast cells, what with the swollen tongue and all. I finally got up to do that thing that other chronically ill people might understand: put on clothes in case I had to go to the hospital. On a normal day, I might sit around in my dressing gown with unbrushed hair all day, but when there could be a chance I’m going to the hospital, I try to make sure I’m not naked. I also make sure I’m not wearing anything I care about — I’ve lost clothes in the hospital before.

Strangely, I had almost an identical episode on this exact day last year. Here’s a screenshot from my calendar:

Screenshot 2019-03-04 at 12

After the most stable autumn and winter I’ve had since being sick, this downturn–this piling on of relatively rare, red-flag symptoms–scares me. My sleep has gone to hell in the last few weeks, which compounds everything by stealing energy and increasing pain. Plus, I’m exacerbating things by holding tight to my “best winter yet” narrative and by fighting so hard to maintain the level of functioning I’ve had this past year, rather than pulling way back and resting aggressively.

My ND says the naturopathic philosophy is that you will go back through previous stages of health and experience earlier symptoms as you travel the healing journey back to where you once were. I’ve latched onto this theory to anchor myself and dispel some fear. The resurgence of all these old symptoms means there has been a shift in my system — but maybe it’s a positive shift, even though it doesn’t feel that way. I’ve gained weight since starting IVIG, over 8% of my norm, which is not insignificant, especially on someone as small as I am. I’m at my heaviest since being sick and, although I’m not overweight, I’ve lost muscle tone the last 7 years and I don’t have the physical ability to burn fat and build muscle, so I hope this trajectory doesn’t continue. My doctor thought this, also, pointed towards a shift in my body: maybe I’ve started absorbing nutrients better. Acne is coming back a little, too. Maybe my hair will grow back! Or the next thing will be that I’ll catch a cold for the first time in 8 years… (And because I really don’t want this to happen, no matter what it might indicate about a calming immune system: knock on wood, toba, toba, spit over shoulder: patuey.)

But, as I lie here, shaky, with my swollen tongue, chronicling these last few weeks (minus the osteoporosis diagnosis and extremely elevated post-antibiotics SIBO test results, both of which I’ll have to write about at a different time), none of it feels like a positive shift and I worry about what I should eat so as not to add to mast cell reactivity and whether I should stay in bed and lie still, even though longed-for Seattle sun is streaming through the windows and I’d love to make some breakfast and sit at my table watching Riley lounge in the grass, soaking up the rays, and the hummingbirds diving around our feeders.

First 911 call since being sick.

We had to call an ambulance this morning for — are you ready for this unbelievable fact? — THE FIRST TIME SINCE I’VE BEEN SICK (absolutely sick and disabled by M.E.; I was fully functional with MCAS for a decade beforehand). And I need the help of all you big brains to figure out the mechanism behind what happened. This is a long post because I want to track exactly what happened. I appreciate your reading this and your thoughts.

My main question is: What can cause sudden bradycardia and loss of consciousness, but not significant hypotension (nor hypertension)? Here’s the back story:

I have a history of anaphylaxis and it almost always happened during my period, usually on the first day, usually after drinking alcohol. I also have a history of collapsing at the start of menstruation, this happened many more times than the full-blown anaphylaxis and often seemed to be triggered by a bowel movement in the morning. The collapsing we’ve called vasovagal syncope, the theory being: vagus nerve triggered by bowel pressure + very reactive day = collapse. I sometimes lost consciousness, but I always was immobile, grey pallor, yellow lips, glazed-over, unfocused eyes, covered in sweat, heavy breathing, hypotensive, bradycardic. What was NOT typical of vasovagal syncope, according to doctors, was that my body didn’t bounce back: my HR did not rise to compensate for the low BP and my BP didn’t come up once I was supine. It usually resulted in ambulance trips to the ER for fluids and at least once I got IV morphine for severe dysmenorhhea (I can’t have any morphine-derived meds anymore).

These were my main health issues before M.E., I felt normal otherwise and pretty much blew them off. Incredibly, they haven’t happened since becoming sick in 2011. My dysmenorhhea actually got much better. Since being sick, I’ve often had bad mast cell reactions and worsening of ME symptoms on the first day of my period, but no collapsing with my husband terrified, calling 911. I thought it was because I’m more conscientious about hydrating and salt-loading.

I was spotting yesterday. My period came on in earnest in the middle of the night, but what disturbed my sleep repeatedly was a viral feeling of sick chills every time I changed positions. Chills and shakes enough to wake me. Then the period cramps started, much, much worse than normal, incredibly painful on the left side. The only thing I could think was maybe it was a ruptured ovarian cyst. I was moaning and crying out with the cyclical cramps, trying to find a position that eased it, my dog Riley clawing at me and burrowing under my body to help. My husband got me a hot water bottle, 2 acetaminophen and a benadryl. Then I took a turn for the worse: I was shaking badly, became nauseous, very weak, drenched in sweat (all the symptoms listed above). We took my vitals: BP was 86/49 (low, but normal for me), temperature was 97 (low, but normal for me), oxygen 96, but my HR was 48 — very abnormal for me. I’m usually 68ish at rest.

My husband got me apple juice in case I was hypoglycemic (it was too much of an emergency situation to check my blood sugar), salt water for my blood pressure, and started to call 911, but I said no. What could they do? Besides charge us thousands of dollars that we don’t have. I’d taken the 2 medications I could take, I could give myself fluids at home with my safe saline, and I didn’t want the two of us sitting around in a building full of flu and measles for hours on end, waiting for blood work and a vaginal ultrasound that would show nothing. But I kept getting worse and knew I was about to lose consciousness (even though I was still in bed and hadn’t even tried to stand up). I was starting to be unresponsive, so my husband called the paramedics.

By the time they got there (3 emergency response vehicles, 6 EMTs!), I’d come back from the edge a bit and was able to talk. They were concerned with my low BP, but I assured them it was normal for me. They did a cursory check of my heart and were concerned about the bradycardia, but said they didn’t see any rhythm issues. They tried to persuade me to go to the hospital, but I said no and signed a waiver. They didn’t want to speculate beyond dehydration (they pointed out that people aren’t realising how dehydrated they are in the current very dry Seattle Snowpocalypse) and possibly needing tests of my reproductive organs. She said, “It’s alarming to lose consciousness while lying down, it’s alarming how low your blood pressure is and it’s alarming that your heart rate isn’t responding to your low blood pressure.” <– That’s what I want to brainstorm.

It was definitely caused by the first day of my period, as usual, but what is the physiological mechanism? What might typically cause sudden bradycardia? What can cause a low HR + low BP (if you take the paramedic’s position)? Or what can cause a low HR + normal BP (if you consider my BP is normally low)? How does a reaction to my period explain this? Could it be 100% pain-induced? If it’s a mast cell reaction, I would expect a high HR and an abnormal BP. Why would I pass out when I’d been lying down the last 9 hours? Why would I pass out with my BP around my normal? Can a low HR cause loss of consciousness without BP dropping significantly? Is this cardiac syncope? Could I have cardiac syncope without knowing I have heart issues? Or autoimmune autonomic dysfunction? Or, once again, adrenal insufficiency? Does losing consciousness usually make breathing labored?

By the time the paramedics left, I was very shaky, but I knew I wouldn’t pass out and my husband helped me get up and hook up my own fluids. I went to bed freezing, with 2 hot water bottles, all my clothes on, under covers in a warm room and it took hours to stop being chilled to the bone (why was I freezing?). When I woke up, finally warm, my HR was 76 — almost 30 bpm higher! I’m still shaky, have a very bad headache, and my heart is jumpy with some palpitations, but completely different from the half-dead, exsanguinated feeling of the bradycardia.

Any ideas are appreciated. I have a routine follow-up appointment with my GP on Tuesday and I’d like to ask her for any tests that might be important. Cardiac work up?

Lastly, I want to mention that it’s REALLY hard not to believe in retaliatory chronic illness gods — yesterday I started writing my first blog update in almost 5 months, it is incredibly positive (“my baseline is higher! I’m able to do more!” etc.) and I stopped myself from writing my usual “gods, cover your ears” and “knock on wood, toba toba” because I’m stable, I’m not as fearful of being knocked down, it’s superstitious nonsense… and then this happens… the first time in 8 years… It just seems a little coincidental. And makes me sad.

Mast Cell Activation May Underlie Chronic Fatigue Syndrome — Medscape

SALT LAKE CITY, UT — Mast cell activation syndrome (MCAS) may be an overlooked yet potentially treatable contributor to the symptoms of chronic fatigue syndrome/myalgic encephalomyelitis (ME/CFS), say physicians who specialize in ME/CFS and its manifestations.

The subject was discussed during a 2-day clinician summit held March 2 to 3, 2018, during which 13 panelists met to begin developing expert consensus guidance for primary care and specialist physicians for the management of the complex multisystem illness ME/CFS, and to recommend research priorities.

“ME/CFS is a descriptive diagnosis of a bunch of symptoms, but it says nothing about what’s causing the symptoms, which is probably part of the reason it’s so hard for it to get recognition. So, the question becomes, What other pathology is driving this illness and making the person feel so ill? I think mast cell activation is one of those drivers, whether cause, effect, or perpetuator, I don’t know,” internist David Kaufman, MD, who practices in Mountain View, California, told Medscape Medical News.

MCAS is a recently described collection of signs and symptoms involving several different organ systems, that, as with ME/CFS itself, do not typically cause abnormalities in routine laboratory or radiologic testing. Proposed diagnostic criteria were published in 2010 in the Journal of Allergy and Clinical Immunology.

Kaufman first learned about MCAS about 5 years ago from a patient who introduced him to the published work of mast cell expert Lawrence Afrin, MD. “I spoke to him and then I started looking for it, and the more I looked, the more I found it,” Kaufman said, estimating that he has identified MCAS in roughly half his patients who meet ME/CFS criteria.

Indeed, summit panel member Charles W. Lapp, MD, who recently retired from his ME/CFS and fibromyalgia practice in Charlotte, North Carolina, told Medscape Medical News, “I see a lot of this. I think it’s one of the many overlap syndromes that we’ve been missing for years.”

Another panel member, New York City ME/CFS specialist Susan M. Levine, MD, also said she sees MCAS frequently. “I suspect 50% to 60% of ME/CFS patients have it. It’s a very new concept.”

In Levine’s experience, MCAS often manifests in patients being unable to tolerate certain foods or medications. “If we can reduce the mast cell problem, we can facilitate taking other drugs to treat ME/CFS,” she said. However, she also cautioned, “It’s going to be a subset, not all ME/CFS patients.”

Clinical Assessment and Laboratory Testing

As discussed at the summit, for patients who meet ME/CFS criteria, the next step is to drill down into individual patients’ symptoms and address treatable abnormalities. Investigation for MCAS may yield such findings among those who exhibit episodic symptoms consistent with mast cell mediator release affecting two or more of the following areas:

  • Skin: urticaria, angioedema, flushing
  • Gastrointestinal: nausea, vomiting, diarrhea, abdominal cramping
  • Cardiovascular: hypotensive syncope or near syncope, tachycardia
  • Respiratory: wheezing
  • Naso-ocular: conjunctival injection, pruritus, nasal stuffiness

Symptoms can wax and wane over years and range from mild to severe/debilitating. It is important to ask about triggers, Kaufman advised. “The patient is usually aware of what makes them feel worse.”

Routine laboratory assessments include complete blood count with differential, complete metabolic panel, magnesium, and prothrombin time/partial thromboplastin time.

More specific laboratory testing can be tricky, as the samples must be kept cold. These include serum tryptase, chromogranin A, plasma prostaglandin D2, histamine, heparin, a variety of random and 24-hour urinary prostaglandins, and urinary leukotriene E4.

For patients who have had a prior biopsy, the saved sample can be stained for mast cells.

Kaufman said that initially after he learned about MCAS, he would only run the laboratory tests in patients with suggestive clinical history, such as food sensitivities/triggers, rashes, hives, temperature intolerance, or chemical sensitivities. “But ultimately, I had patients [for whom] I couldn’t figure out what was going on; I would check, and started finding positives in patients I wasn’t suspicious of.”

So, now he just tests for it in all his patients with ME/CFS. “It’s bigger than allergy,” he remarked.

Treatment May Ease Some ME/CFS Symptoms

Treatment of MCAS involves trigger avoidance as possible; H1 receptor antagonists such as loratadine, cetirizine, or fexofenadine (up to double the usual doses); H2 histamine receptor antagonists including famotidine or ranitidine; and mast cell membrane-stabilizers such as cromolyn sodium. Slow-release vitamin C can also help in inhibiting mast cells.

Over-the-counter plant flavonoids such as quercetin also may be helpful, typically at high doses (up to 1000 mg three times daily). “There’s a long list of medications that either quiet down mast cell activation or block the receptor,” Kaufman noted.

But despite that, without controlled trials, it is difficult to determine the exact clinical effects of blocking mast cells, especially as these patients tend to be taking many other medications. And in the context of ME/CFS, the extent to which suppressing mast cell activity addresses the core symptoms of fatigue, postexertional malaise, orthostatic intolerance, and cognitive dysfunction is unclear.

Kaufman noted, “I think treatment clearly helps with the fatigue because they’re not reacting to everything. It improves gastrointestinal symptoms, so they can eat better…. I have seen [postural orthostatic tachycardia syndrome] improve, but I have to say I also give meds for dysautonomia, so I can’t be sure.”

Lapp said that in his experience, “[Patients with ME/CFS] aren’t cured, but do get better. [Blocking mast cell activity] gets rid of dizziness, fatigue, nausea, and light sensitivity.”

Levine pointed out, “We’re just at the beginning of identifying this patient subset and thinking what makes sense to try…. One thing that’s sure is that the drugs are pretty safe,” she said, adding that when it comes to working up patients with ME/CFS for MCAS, “There only seem to be good things that can happen.”

Long Overdue Update

I think it’s time to write an update. I haven’t wanted to neglect my blog — in fact, I wake up daily thinking about things I’d like to document and share — but I’ve somehow been very busy for what feels like years. My energy is still so limited and, with each incremental increase in functioning, I want to take some of the burden off my husband by cooking my own food, getting myself to appointments or taking care of our dog. It leaves no space for writing. I hesitate to say “no time for writing” because, even as a sick person — even as the person in question — I think, “you have nothing but time!” But I don’t, my window of functionality is still so small. There were months in the past when I worked 70 hours a week and I somehow still had the time to accomplish more than I do now — because my internal engine worked efficiently and my tank held much more gas and was easily refilled overnight. I can imagine my healthy friends reading this and wondering how someone with no job, no kids and no social engagements can possibly feel like they don’t have time to write an update. Maybe, if I manage to complete this blog post, it’ll be clearer.

These last few years, I have put great effort into trying to be an easier human to be around, trying to act like my old self for my husband and when I see people — you know, trying to be one of those “it’s great the way she stays positive and keeps fighting while dealing with such suffering” kind of people. But when you only post the good moments on Facebook and you draw from deep reserves while talking to people to appear perky and mildly engaging, it can cause… confusion, for lack of a better word. Even my closest friends and family obviously can’t see on the outside of me what I assume must be alarmingly salient and sometimes I get concerned that maybe, deep down, they think I’m just living the good life while my husband slogs away at his very physically-demanding job. They have made comments that make me think I’ve never done a good job of explaining this disease and, in fact, sometimes their loving and well-meaning encouragement sounds like they think I need the courage to get out into the world.

There are certain things that take courage in my life– they are all mast cell threats. It takes courage for me to go to places where there are no easily-accessible emergency rooms, like Vashon Island, where our friends live, or in an airplane. It takes courage to try a new medication, knowing I could have a reaction. My experiences with full-blown anaphylaxis and nocturnal mast cell meltdowns have made me fearful of a lot in life — not only of things I’ve reacted to, but typical triggers that have never caused me problems because I always wonder if they’re filling my “bucket” and the reaction is looming behind a blind bend in the road. For example, I may think I can eat just about anything and I love hot weather, but most mast cell patients can’t and don’t. So, maybe a few family members come over on the 4th of July and my period is due (“events” can cause reactions for me, as does menstruation). I’m basking in the sun and I’ve eaten a banana, some cheese, some chocolate that day (typical foods that cause reactions for others). Then the fireworks start and my dogs go into paroxysms of panic, which causes me distress (emotions can degranulate mast cells) and, just like that, the bucket overflows and my tongue swells up and I’m in for a very scary, sleepless night. I think it’s just from hormones and excitement, but maybe without the sunbathing or the chocolate, it wouldn’t have happened, who knows? I’ve been blindsided by this sort of thing too often and it seems, no matter how much time goes by, there will always be a tad bit of trepidation lurking in the back of my mind when navigating the minefield of mast cell degranulation.

So, some things do take courage, yes, but living, doing, experiencing, independence — all the things that ME/cfs took from me — they take no courage at all, they just need a functioning body. My greatest desire is to be traveling or socialising or hiking with my dog. If I was suddenly healed tomorrow, all of your phones would be ringing off their hooks and I’d be asking to crash on your couches as I hopped from Seattle to Oregon to California to Wisconsin to Tennessee to New York to Connecticut to Ireland to England to Germany and hugged you all close and talked your ears off for months on end. If anything, I need to be urged to pull back and conserve my energy because I am my own worst enemy, suffering payback on a daily basis from some reckless endeavor like cutting a thick-skinned squash or shaving my legs. Yesterday, I took Riley and my sister-in-law’s dog on a walk, using my mobility scooter. When I used to take Bowie out, it took very little strength and energy: He could be off-leash, I’d sit on the scooter and watch him eat grass or motor beside him as he ambled along. But these two pups are runners, pullers, criss-crossers and leash-tanglers. Not only did our hour walk sap the majority of my energy yesterday, today I am in pain from head to coccyx from using muscles that I usually don’t. But it brings me such joy, of course, so I’ll do it again.

For about four months this year — mid-April to mid-August — I was probably better than I’ve been since getting sick. But, when my Mum visited last March she said it was the sickest she’d ever seen me. It wasn’t — I think she has forgotten some of the horrors of the early years — but that illustrates just how changeable my health can be in a 6-month period. In general, if I keep my activity steady, I can predict how my days will go. That doesn’t mean I can control how severe my symptoms are, it just means that the worse I get, the less I do each day and vice versa and, if I’m careful, this will usually even out to a higher or lower baseline. In the beginning of my chronic illness, the freefall didn’t slow until I stopped working, then stopped going out of the house and eventually spent most of my time in bed. Slowly, slowly thereafter, my days became more predictable and then, even slower than that, my limits expanded, millimeter by millimeter.

Besides managing my activity, I think the only other thing that has contributed to my improvements are immunoglobulin infusions, which I’ve been doing for three years. But, like I said, I was much sicker last winter while still doing infusions, so you can always assume that those two steps forward will be followed by one step back. Just as long as there is a net profit at the end of the year, I’m content. Not happy or at peace, but I’ll take it.

Anyway, on to the actual update. But I’m wiped now, so to be continued…

Dental Work Protocol and Precautions for People With MCAS/ME/MCS.

I have to get a filling done for the first time since being sick and extremely reactive to medications. I know this is the beginning of many future dental procedures because I have a lot of aging mercury fillings and I’m sure they will have to be replaced eventually. Also, I haven’t been wearing any sort of oral device when I sleep — be it a night guard or apnea apparatus — so I’ve been clamping down, grinding and cracking my teeth again. Also, my teeth feel more unstable this past year: I have trouble chewing certain foods in certain spots and random pain. I read that this might be a result of immunoglobulin infusions; some people claim it wrecks dental health. I haven’t gone down that research rabbit hole, but it nags at me a bit. So, I need to find out what anesthetics and materials are safe for me and develop a standing protocol for this current cavity and also for future dental work.

I am one of these mast cell people that can eat almost anything, but I have extreme reactions to micro-doses of medications — even medications I’ve taken with no problem in the past — so, I’m scared of being in a dentist’s chair and having an anaphylactic reaction of any sort. I’ve been doing research and, as usual with MCAS, there aren’t great ways to control the outcome of a procedure like this besides taking normal precautions and crossing my fingers. Normal precautions for me are:

  • Schedule my appointment for a safe time of the month. My menstrual cycle is bananas at the moment (has been coming every 13 days some months recently and spotting daily), so I only feel confident the first week after my period.
  • Premedicate: For the week before, I will not forget to take my Loratadine and Ranitidine twice a day. On the day of, I will take Prednisone (I take a VERY low dose because it wallops me), Benadryl, Zantac and Paracetamol.
  • Hydrate to raise blood pressure: In the days before, I will drink 2-3 litres of water. On the day of, I will do IV fluids (maybe).
  • Food to stabilize blood sugar: Be well fed before the procedure and have frozen food prepared for afterwards. I also eat a lower histamine diet in the days before and after a new or risky medical procedure.
  • Rest: Be well rested before and proactively rest after the procedure.
  • Try to do as much of the dental work as possible without anesthetic. Before the dentist starts, bite open a capsule of Benadryl and squirt it on the tooth and gums in question. I learned this trick from an allergist who told me to squirt Benadryl directly on my tongue when it swelled up. Benadryl is a great numbing agent.
  • Have the dentist use a local anesthetic without epinephrine. I found this out the hard way long before I was sick or dealing with mast cell issues. I’ve always responded badly to epi.
  • I always carry salt packets, glucose tablets, electrolyte water, antihistamines and an EpiPen to help stabilse my vitals, manage any reactions and ward off vasovagal syncope.

Once I’ve gotten this first filling out of the way with no reactions, I’ll undoubtedly ease up on the pre-meds and not consider IV fluids, but, because I don’t know how I’ll react, I’m taking all precautions this time.

Here is some info on choices for dental materials:

  • Local anesthetics:
    • Allergic reactions to local anesthetics may occur as a result of sensitivity to:
      • 1) either the ester or amide component;
      • 2) the preservative methylparaben;
      • 3) sulfites (sodium bisulfite, potassium metabisulfite), which are used as a preservative in local anesthetics that contain epinephrine; or
      • 4) the medication, itself.
    • Ester-based local anesthetics are typically associated with a higher incidence of allergic reactions due to one of their metabolites, para-amino benzoic acid (PABA). In general, amide-based local anesthetics are less likely to cause allergic responses because they do not undergo metabolism to PABA.
    • Ester-based injectable local anesthetics are no longer used in the United States, but are used topically (numbing jellies, such as Benzocaine), so discuss what your dentist will be using.
    • Allergic reactions to amide-based local anesthetics can occur because of the preservative, methylparaben, which is structurally similar to PABA. However, methylparaben has been removed from single-use dental local anesthetic cartridges, which are what private dental offices typically use (multi-use vials might still contain methylparaben. These are typically used in hospital settings and physicians’ offices). Double-check what your dentist uses.
    • True allergies to amides are exceedingly rare in the general population (but they do exist — for some ideas on how to navigate dental work with an amide allergy, see this article). Because of this, your dentist might (correctly) tell you that allergies to amides (as opposed to the preservatives in the anesthetic) are virtually unheard of or that it is impossible to be “allergic” to epinephrine. I think it’s important not to use the word “allergy” too casually, but, rather, make sure your doctor understands how mast cell degranulation works with MCAS: that you can have anaphylactic (life-threatening) reactions that are not IgE-mediated, but present the same way.
    • People with ME, mast cell disease or multiple chemical sensitivity (MCS) often have exaggerated reactions to the epinephrine in many local anesthetics. These anesthetics also contain sulfites (added as a preservative for the epinephrine), which can cause allergic reactions. If you are concerned about reactions to epi, sulfites or want to play it safe, I would ask for a local anesthetic without epinephrine. Bear in mind, you will metabolize the anesthetic quicker than if it had epinephrine, so, depending on the procedure, you may need more injections (right before I got sick, I had dental work done that required over 20 injections and I think the gruelling nature of that day probably played a part in my immune system crash).
    • Examples of common anesthetics that are typically tolerated, according to The Mastocytosis Society: Lidocaine, Bupivacaine, Prilocaine (brand names Bidanest or Citanest Plain (the latter contains no vasoconstrictor)), Mepivacaine (also called Carbocaine, Scandonest, Polocaine (by Astra)) and Ropivacaine (which is always preservative-free). I believe Mepivacaine is always free of epinephrine (and I’ve been told by a few friends that they had no reactions to it; one very sensitive friend specified that she got 3cc of 1.7% Carbocaine and was fine), but, as always, double-check with your dentist. This page has a handy chart of local anesthetics’ ingredients.
    • Some anesthetics don’t use epi, but do use a different vasoconstrictor (for example, Citanest Forte), so make sure you are clear on what your dentist uses.
    • Other things to note:
      • If you have Ehlers-Danlos Syndrome (EDS), which is a connective tissue disease that is a common comorbid condition of ME, MCAS and POTS/dysautonomia, you might need more anesthetic and it might wear off quicker than the average person — especially when using a medication without epinephrine because there’s no vasoconstriction.
      • Vasodilators are risky for those of us with hypotension and circulatory problems. Nitrous oxide is a cerebral vasodilator — not to be confused with NITRIC oxide (not used in dentistry, as far as I know), a strong vasodilator often used for respiratory diseases.
      • Most topical anesthetics contain gluten, so those individuals with either celiac disease or gluten sensitivity should avoid topical anesthesia.[ii]
      • I have been told by multiple people with chronic pain syndromes that going without anesthesia is not a good idea because, in these cases, the body “remembers” the pain and it can set you up for future worsening issues.
  • Fillings:
    • Composite: cheaper, expands better than porcelain, usually better for small fillings.
      • Traditional composite examples:
        • Grandioflow
        • Filtek Supreme Ultra by 3M
      • Holistore unshaded by DenMat is a biocompatible composite that is recommended for bonding and smaller fillings. It contains no metal oxides, but is quite white in color and is significantly less durable than some other composites. Premise Indirect (formally BelleGlass) unshaded by Kerr for in a metal-free composite that can be used for crowns, inlays and bridges.
    • Porcelain: looks more natural than composite and the consensus is that this is the safest material option, however porcelain contains more metal oxides than composite and is much more expensive ($thousands vs $hundreds). It cannot be used in certain instances (for example, small spaces between teeth). They are pre-fabricated, so take more time and multiple appointments.
      • Inlays: fit inside the tooth.
      • Onlays: fit over the tooth.
      • Crowns and bridges.
      • Zirconium: can be used for inlays/onlays or implants.
  • Dental cements/adhesives/bonding agents: There are various different kinds (for example, my dentist uses Prime & Bond Elect by Dentsply and Relyx is often used for crowns). Some biological dentists recommend Tenure and Tenure S by DenMat for bonding. Other brands used by bio-dentists I’ve contacted: Optibond, Admira Bond, All Bond Universal. Like composite material, there’s not a lot of information on brands that are “safer”, so you might just have to try one out and cross your fingers.

Dr. Douglas Cook, who is known to see many patients with MCS, has written books and has a lot of info on his website about biocompatible dental materials.

Here’s a link to the most typical dental materials that test as “clean” and relatively inert.

For an good in-depth analysis, see this article: Allergic Reactions to Dental Materials-A Systematic Review.

There are options for reactivity testing before you have dental work done. I’m a bit of a skeptic and, more importantly, I like to conserve energy and money, so I probably won’t do any of this testing, but I’ll lay them out:

Testing before dental work (some info here):

  • Clifford blood test: You need a doctor to order this test and it’s over $300. It tests for “antibody sensitivity” to 94 chemical groups and “correlates” these sensitivities to 17,204 dental materials. I put those in quotes because, after corresponding with Walter Clifford and researching how these tests are done, I’m not sure I trust his skills or the accuracy/scientific legitimacy of the testing. IMHO. I might be wrong. However… it’s something. It’s a guide. Even if, at a minimum, it makes a patient feel more confident and less fearful of a reaction, that, in itself, can calm mast cells. (Note: If you do immunoglobulin infusions, the accuracy of the Clifford test results will be compromised.)
  • Muscle testing dental materials. Biological dentists often have kits that can be sent to your ND. Again, I’m not sure how I feel about muscle testing, but, at the very least, it’s a way to provide direction and give confidence.
  • MELISA blood test for metal allergies. You need a doctor’s order and they’re pricey. Here is their test requisition with the costs. Shipping to Germany from where I live is $118 on top of the cost of the test, so bear this in mind.

It turns out, my cavity has grown around an existing mercury filling, which will have to come out. I was planning to go to my regular dentist (who is interested in learning about mast cell diseases and is phenomenal about talking through options), but he doesn’t take any precautions when removing mercury and the last thing I need is my body to be burdened by additional toxins when I am compromised in virtually every detoxification pathway there is (not just things like liver and methylation, but my body doesn’t even manage to do the very basics like bowel movements and sweating). So, I’m planning on finding a local dentist that practices the “SMART” protocol for mercury removal. The downside of this is that I’ll need another full exam with my new dentist even though I just had one with my regular dentist, which means at least two appointments to get the filling done. Plus, this is all out of pocket for me, but my regular doctor gives me a cash discount which these holistic/biological dentists don’t = energy and $$$.

You can search here, but I asked my doctor, my friends and in local online groups and came up with this list of Seattle-area dentists:

  • Paul Rubin (North Seattle, possibly retiring soon)
  • Richard Stickney (downtown, front office staff is incredibly informative, thorough and kind)
  • Jessica Saepoff (Issaquah and Mercer Island)
  • Rebecca Taylor
  • Gregory Zimmer (Tacoma)
  • Mitch Marder (I ruled him out for myself because of a bad experience.)

I think I am going to see Paul Rubin or Richard Stickney, based on location and my conversations with their staff. I’ll let you know how it goes.

Speaking of detox, you might want to consider taking/using these things before and after dental work (I never have, but I’m considering it):

  • Charcoal capsules
  • Charcoal toothpaste
  • Chlorella
  • DMSA
  • One dentist recommended taking this product up to a month before mercury removal.

See The Mastocytosis Society’s medication guide here and more on medications that impact mast cell degranulation here.

Find mast cell dental info on Lisa Klimas’s Mast Attack blog here and other articles by Cathy Scofield here and here. An ME/CFS dental info handout is here.*

*I did not write these articles or research the details, so some of the info might not be entirely accurate — it’s up to you to do your own research.


The Mastocytosis Society’s Emergency Room Protocol.
[i] Allergic Reactions Did you know. . . Volume IV, Number 1 | January/February 2001
[ii] “Numbing Jelly” or Dental Topical Anesthesia.
Understanding allergic reactions to local anesthetics.
Allergic Reactions to Dental Materials-A Systematic Review.
Non-IgE mediated mast cell activation.
Novocaine Allergy Part II – Methylparaben and Sulfites.