| Reason for care | Post op care |
| Role of mast cells | Mast cells are inherently activated following surgery as they drive tissue remodeling, angiogenesis, and wound repair.[i]
Mast cells are involved in the transmission of pain stimuli.[iii] |
| Impact of condition on mast cells | Mechanical trauma or pressure, such as dressing a wound or palpating the area, can directly induce degranulation and mast cell activation[ii].
Pain can trigger mast cell activation.[iii] Psychological and physical stress can trigger an inflammatory response that involves mast cell activation.[iv] |
| Notes regarding condition treatment | NSAIDS can trigger mast cell degranulation and cannot be taken by some mast cell patients.[iv]
Codeine and derivatives can trigger mast cell degranulation[v]. Vancomycin, gyrase inhibitors and cefuroxime should be avoided where possible due to risk of mast cell activation.[vi] Amide caine anesthetics are preferred over ester caines.[vi] ACE inhibitors and β-adrenergic receptor antagonists (beta blockers) should be avoided. In particular, beta blockers directly interfere with the action of epinephrine and can impede anaphylaxis management.[vi] Fentanyl and fentanyl derivatives are the preferred narcotic for mast cell patients due to low risk of degranulation. Hydromorphone and oxycodone are suggested by some authors and see use in mast cell patients.[vi] Benzodiazepines can provide anxiolytic and anticonvulsive support in mast cell patients are needed.[vi] IV contrast poses significant to mast cell patients due to the high risk of systemic degranulation. If required, premedication is advised.[vi] Adhesive allergy is not unusual and patients may require specific occlusive dressings, tapes, or wound glue. |
| Notes regarding mast cell treatment | Antihistamines and mast cell stabilizers can be helpful in mitigating common post op symptoms such as opiate induced itching and nausea. COX inhibitors can help with pain management.[vii] |
| Special considerations for mast cell patients | Mast cells are the largest reservoir of endogenous heparin. Patient should be monitored for coagulopathy.[viii]
Mast cells contribute significantly to post operative ileus.[ix] Intestinal manipulation directly results in mast cell degranulation.[ix] |
| Reason for care | Hypertension |
| Role of mast cells | Mast cell mediators can impact blood pressure. Histamine acting on H2 receptor can promote hypertension.[xi]
Renin, chymase, and carboxypeptidase A all participate in hypertension by dysregulation of angiotensin II.[xi] 9a,11b-PGF2, the degradation product of prostaglandin D2, thromboxane A2, and leukotrienes increase blood pressure.[xi] |
| Impact of condition on mast cells | Dysregulation of angiotensin II and renin levels can affect mast cell behavior.[x] |
| Notes regarding condition treatment | ACE inhibitors and β-adrenergic receptor antagonists (beta blockers) should be avoided. In particular, beta blockers directly interfere with the action of epinephrine and can impede anaphylaxis management. Alternatives include calcium channel blockers, renin inhibitors, and ivabradine, among others.[vi] |
| Notes regarding mast cell treatment | Several mast cell medications can impact levels of histamine, renin, and angiotensin II, all of which can affect blood pressure. |
| Special considerations for mast cell patients | Mast cell patients taking β-adrenergic receptor antagonists (beta blockers) should carry a glucagon pen to increase efficacy of epinephrine in anaphylaxis.[xi]
As many as 31% of patients with mast cell disease demonstrate elevated arterial blood pressure secondary to mast cell activation. These elevations may be episodic or chronic.[xi] Mast cell patients may also have hyperadrenergic postural orthostatic tachycardia syndrome (hyperPOTS), a condition that can cause hypertension.[xii] |
| Reason for care | Heart disease |
| Role of mast cells | Renin, chymase, and carboxypeptidase A all participate in hypertension by dysregulation of angiotensin II, contributing to evolution of arrhythmia.[xi]
Prostaglandin D2, VIP, PAF, IL-6 and nitric oxide are all vasodilating and can contribute to tachycardia.[xi] Tryptase, histamine, PAF, IL-10, TNF, IL-4, IL-6, FGF, and TGFB can contribute to heart failure.[xi] Mast cells participate in the formation, destabilization and rupture of atherosclerotic lesions.[xiii] Histamine release is associated with acute coronary syndromes such as Kounis Syndrome, commonly known as “allergic MI” or “allergic angina”.[xiv] Leukotriene C4, adrenomedullin, tryptase and chymase participate in the formation, destabilization and rupture of aneurysms.[xiii] |
| Impact of condition on mast cells | Heart disease, especially heart failure, can disrupt release of catecholamines including norepinephrine.[xv] Norepinephrine dysregulation can impact mast cell behavior.
Dysregulation of angiotensin II and renin levels can affect mast cell behaviorx |
| Notes regarding condition treatment | NSAIDS can trigger mast cell degranulation. Some mast cell patients are unable to take them.xx
Acetaminophen is generally recommended for use in mast cell patients.[iv] ACE inhibitors and β-adrenergic receptor antagonists (beta blockers) should be avoided. In particular, beta blockers directly interfere with the action of epinephrine and can impede anaphylaxis management. Alternatives include calcium channel blockers, renin inhibitors, and ivabradine, among others.[vi] |
| Notes regarding mast cell treatment | COX inhibitors are routinely taken by mast cell patients and may provide relief of prostaglandin induced symptoms.[vi]
Several mast cell medications can impact levels of histamine, renin, and angiotensin II, all of which can affect blood pressure. Epinephrine can provoke myocardial ischemia, prolong QT interval, and exacerbate coronary vasospasm and arrhythmia.[xiv] |
| Special considerations for mast cell patients | Over 20% of systemic mastocytosis and mast cell activation syndrome patients experience palpitations and supraventricular tachycardia.[xi]
Prostaglandin D2 can cause tachycardia. PGD2 is associated with late phase allergic response and symptoms may be delayed for several hours after allergic event.[xi] One study showed that 12/18 mast cell activation syndrome patients showed diastolic left ventricular dysfunction.[xi] Mast cell patients may also have postural orthostatic tachycardia syndrome (POTS), a condition that can cause blood pressure and heart rate irregularities.[xii] |
| Reason for care | Chest pain |
| Role of mast cells | Mast cells participate in the formation, destabilization and rupture of atherosclerotic lesions.[xiii]
Histamine release is associated with acute coronary syndromes such as Kounis Syndrome, commonly known as “allergic MI” or “allergic angina”.[xiv] Leukotriene C4, adrenomedullin, tryptase and chymase participate in the formation, destabilization and rupture of aneurysms.[xiii] Mast cells participate in esophageal inflammation in several models, including from acid reflux.[xvi] Mast cells contribute to GI dysmotility which can cause esophageal spasms.[xvii] Mast cells are involved in the transmission of pain stimuli.[iii] |
| Impact of condition on mast cells | Pain can trigger mast cell activation.[iii]
Psychological and physical stress can trigger an inflammatory response that involves mast cell activation.[iv] |
| Notes regarding condition treatment | NSAIDS can trigger mast cell degranulation. Some mast cell patients are unable to take them.xx
Acetaminophen is generally recommended for use in mast cell patients.[iv] Fentanyl and fentanyl derivatives are the preferred narcotic for mast cell patients due to low risk of degranulation. Hydromorphone and oxycodone are suggested by some authors and see use in mast cell patients.[vi] Benzodiazepines can provide anxiolytic and anticonvulsive support in mast cell patients are needed.[vi] ACE inhibitors and β-adrenergic receptor antagonists (beta blockers) should be avoided. In particular, beta blockers directly interfere with the action of epinephrine and can impede anaphylaxis management. Alternatives include calcium channel blockers, renin inhibitors, and ivabradine, among others.[vi] |
| Notes regarding mast cell treatment | COX inhibitors are routinely taken by mast cell patients and may provide relief of prostaglandin induced symptoms.[vi] |
| Special considerations for mast cell patients | Mast cell patients may experience GI dysmotility which can cause esophageal spasms.[xviii]
Mast cell patients sometimes have eosinophilic esophagitis, causing esophageal spasms, food impaction, and pain.[xix] Over 20% of systemic mastocytosis and mast cell activation syndrome patients experience palpitations and supraventricular tachycardia.[xi] Prostaglandin D2 can cause tachycardia. PGD2 is associated with late phase allergic response and symptoms may be delayed for several hours after allergic event.[xi] One study showed that 12/18 mast cell activation syndrome patients showed diastolic left ventricular dysfunction.[xi] Mast cell patients can present with Kounis Syndrome. Management of Kounis Syndrome relies upon addressing both cardiovascular aspects of the episode as well as allergic aspects.[xiv] Costochondritis can occur in mast cell patients and may present as chest pain. Mast cell patients may also have postural orthostatic tachycardia syndrome (POTS), a condition that can cause blood pressure and heart rate irregularities.[xii] IV contrast poses significant to mast cell patients due to the high risk of systemic degranulation. If required, premedication is advised.[vi] |
References:
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[ii] Zhang D, et al. (2012). Mast-cell degranulation induced by physical stimuli involves the activation of transient receptor-potential channel TRPV2. Physiol Res, 61(1), 113-124.
[iii] Chatterjea D, Martinov T. (2015). Mast cells: versatile gatekeepers of pain. Mol Immunol, 63(1),38-44.
[iv] Dewachter P, et al. (2014). Perioperative management of patients with mastocytosis. Anesthesiology, 120, 753-759.
[v] Brockow K, Bonadonna P. (2012). Drug allergy in mast cell disease. Curr Opin Allergy Clin Immunol, 12, 354-360.
[vi] Molderings GJ, et al. (2016). Pharma,ological treatment options for mast cell activation disease. Naunyn-Schmiedeberg’s Arch Pharmol, 389:671.
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[viii] Carvalhosa AB, et al. (2015). A French national survey on clotting disorders in mastocytosis. Medicine (Baltimore), 94(40).
[ix] Peters EG, et al. (2015). The contribution of mast cells to postoperative ileus in experimental and clinical studies. Neurogastroenterol Motil, 27(6), 743-749.
[x] Biscotte SM, et al. (2007). Angiotensin II mediated activation of cardiac mast cells. The FASEB Journal, 21(6).
[xi] Kolck UW, et al. (2016). Cardiovascular symptoms in patients with systemic mast cell activation disease. Translation Research, x, 1-10.
[xii] Shibao C, et al. (2005). Hyperadrenergic postural tachycardia syndrome in mast cell activation disorders. Hypertension, 45, 385-390.
[xiii] Kennedy S, et al. (2013). Mast cells and vascular diseases. Pharmacology & Therapeutics, 138, 53-65.
[xiv] Kounis NG. (2016). Kounis Syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management. Clin Chem Lab Med, 54(10), 1545-1559.
[xv] Florea VG, Cohn JN. (2014). The autonomic nervous system and heart failure. Circulation Research, 114, 1815-1826.
[xvi] Morganstern JA, et al. (2008). Direct evidence of mast cell participation in acute acid-induced inflammation in mice. J Pediatr Gastroenterol Nutr, 46(2), 134-138.
[xvii] De Winter BY, et al. (2012). Intestinal mast cells in gut inflammation and motility disturbances. Biochimica et Biophysica Acta – Molecular Basis of Disease, 1822(1), 66-73.
[xviii] De Winter BY, et al. (2012). Intestinal mast cells in gut inflammation and motility disturbances. Biochimica et Biophysica Acta – Molecular Basis of Disease, 1822(1), 66-73.
[xix] Nurko S, Rosen R. (2010). Esophageal dysmotility in patients with eosinophilic esophagitis. Gastrointest Endosc Clin N Am, 18(1), 73-ix.