Child and Chest Health Care Delhi NCR

• Anaphylaxis a potential life threatening condition.
• It is defined as a medical condition,which is rapid in onset(minutes to hours),allergic in nature and may culminate into death if left untreated.
• It is charachterised by acute onset urticaria,pruritus,edema of the face,lips,uvula,larynx with respiratory,cardiovascular,and gastrointesninal symptoms.
• It is very difficult to recognise the symptoms of anaphylaxix in infants as few symptoms like excessive cry with sudden calmness,excessive fussiness and excessive swaeting may be observed in infants not suffering from anaphylaxix.Moreover,infants can not express their symptoms.
• Majority of anaphylaxis have been observed in children rather than adults,all over the world.
• Most common allergen leading to anaphylaxis in children is food allergen.
• Most common food allergens are peanut,treenut,shellfish,egg and milk.
• Food preservatives,additives,coloring agents,and spices are potential allergens
• Galactose which is found in meat may be an allergen and the allergic manifestations due to it, may take 4-6 hours to appear.
• Some food allergens cause allergic reactions only after exercise ,when exercise is performed within 3-4 hours after taking meals.
• Some children are allergic to latex being used to manufacture gloves used for various procedure in hospital.
• Allergic reactions may be mediated through IgE or non IgE like IgG mediated in case of high molecular weight dextran use and direct release of mediators from cells after exercise.
• The incidence of anaphylaxis has increased enormously all over the world in last 2 decades.

DIAGNOSTIC CRITERIA:Any one of the following three ,makes it a diagnosis of anphylaxis-

1.Onset within minutes to hours(ACUTE) of generalised  itching,hives,swelling of lips,uvula,tounge and flushing(INVOLVEMENT OF SKIN AND/OR MUCOSAL TISSUES)  and one of the following two-

a.breathlessness,wheeze,bronchospasm,stridor.hypoxemia,reduced PEF(RESPIRATORY COMPROMISE)

b.Low blood pressure for the age or symptoms of end organ dysfunction in the form of collapse,hypotonia,incontinence or syncope.(HYPOTENSION)

2.Two or more of the following four:

a.Generalised involvement of skin and/or mucosal tissues

b.Respiratory compromise

c.Reduced blood pressure for the age or symptoms of end organ failure

d.Crampy abdominal pain,vomiting which is persistent(PERSISTENT GASTROINTESTINAL SYMPTOMS)

3.Low blood pressure

a. For infants one month to 12 months, systolic BP less than 70mm of Hg and  for children 1 year to 10 years Systolic BP less than 70+age in years OR >30% drop in systolic BP

b.For adults ,systolic BP <90mm of Hg OR >30% drop in systolic BP

ESSENTIAL CRITERIA IS ,THE ABOVE FEATURES SHUOLD BE INTERPRETED ONLY AFTER EXPOSURE TO KNOWN OR LIKELY ALLERGEN.

 

Triggers of anaphylaxis:Foods,medicines,vaccines,immunotherapy,insect venoms,latex,cold exposure and exercise.

IT MAY BE IDIOPATHIC

WHAT HAPPENS IN THE BODY(Pathogenesis): The main process is the release of mediators like histamine and  tryptase and cytokines from the cells like mast cell and basophils and possibly from macrophages. These mediators and cytokines produce allergic symptoms in whole body.

The release of these chemicals may be  IgE dependent or non IgE dependent.In case of IgE dependent, the child  must be exposed previously to an allergen which produces allergen specific antibody(IgE) which gets bound to mast cells. Upon reexposure these mast cells which are bound to IgE start releasing histamines and tryptase which is responsible for the symptoms.

Anaphylaxis may also be caused by release of mediators by the process than IgE mediated like direct release by medication like morphine,by physical factors like cold and exercise,disturbance of leukotriene metabolism like after use of aspirin and non steroidal anti inflammatory drugs,immune aggregates and complement activations like after ithe use of blood products,probably by complement activation like after the use of radiocontrast dyes and IgG mediated reactions like arter the use of humanised monoclonal antibodies and chimeric.

Pathological features are: airway obstruction,pulmonary edema  alveolar hemorrhage,visceral congestion ,laryngeal edema and angioedema. Vasomotor dilataton and/or cardiac dysrhythmia is responsible for hypotension (low BP)

INVESTGATIONS: It is a clinical diagnosis.No investgation is reliable,although serum tryptase level may be raised for several hours but not in food allergy.

TREATMENT:The mainstay of treatment is epinephrine(adrenaline).

 

It comes in the market in injectable form in 1ml ampoule of 1:1000 strength.It shuold be kept at around the temeratue of 25dC.It should be injected undiluted intramuscularly in lateral thigh in the dose of 0.01ml/kg upto a maximum of 0.5ml(1ml=1mg).It can be repeated at an interval of 5 to 15 minutes twice if symptoms persist and intravenous line has not been established.In case of persistent symptoms i.v line should be established and adrenaline drip should be started.For i.v. use the injection must be diluted to 1:10000 strength. In case of non establishment of i.v. line ,it can be given through endotracheal or intraosseous route.

Patient should be kept in supine position with leg end raised in case of hemodynamic compromise.

In case of non response,oxygen inhalation should be started after estalishing airway,N/S or R/L should be given in the dose of 30ml/kg over one hour if BP is low and salbutamol nebulisation should be given if there is bronchspasm.

In case of non responders specially in the users of beta blockres, glucagon should be used and for bronchodilation ipratropium should be used. Some patients may require vasopressin and in case of asystole and pulseless electrical activity atropine should be used.

Other drugs being used are: HI blocker-cetrizine in the dose of 0.25mg/kg upto a maximum of 10 mg  orally or Diphenhydramine in the dose of 1.25mg/kg upto a maximum of 50 mg orally or IM,H2blocker-ranitidine and corticosteroids

Crticosteroid-The dose of methyleprednisolone is 1-2mg /kg i.v upto a maximum dose of 125mg.(SOLUMEDROL)

Inramuscular dose is 1mg/kg upto a maximum of 80mg(DEPOMEDROL)

CAUTION:1. Rapid i.v. infusion or incorrect strength during i.v. use of adrenaline may cause pulmonary edema,hypertension and myocardial infarction

2.Rapid i.v. infusion of ranitidine may cause hypotension

Some patients may experience biphasic anaphylaxis. In this phenomenon,the features of anaphylaxix reappears after clinical resolution. In more than 90% of cases,it happens within 4 hours. So patients must be observed for at least 4 hours before discharge.

MANAGEMENT AFTER DEALING WITH EMERGRNCY:Antihistamine should be given for 3 days and it is optional to prescribe 3 days of oral corticosteroid.

REFERENCES:

Sampson, HA, Muñoz-Furlong, A, Campbell, RL. J Allergy Clin Immunol. vol. 117. 2006. pp. 391-7.

(A summary of the second international conference to develop a universally accepted definition of anaphylaxis, establish clinical criteria that would accurately identify cases of anaphylaxis with high precision, and review the evidence on the most appropriate management of anaphylaxis.)
Simons, FE. “Pharmacologic treatment of anaphylaxis: can the evidence base be strengthened”. Curr Opin Allergy Clin Immunol. vol. 10. 2010. pp. 384-93.

Sheikh, A, Shehata, YA, Brown, SG, Simons, FE. “Adrenaline for the treatment of anaphylaxis: Cochrane systematic review”. Allergy. vol. 64. 2009. pp. 204-12.

Sheikh, A, Ten Broek, V, Brown, SG, Simons, FE. “H1-antihistamines for the treatment of anaphylaxis: Cochrane systematic review”. Allergy. vol. 62. 2007. pp. 830-7.

Choo, KJ, Simons, FE, Sheikh, A. “Glucocorticoids for the treatment of anaphylaxis”. Cochrane Database Syst Rev. 2010 Mar 17. pp. CD007596.

Pumphrey, RS. “Lessons for management of anaphylaxis from a study of fatal reactions”. Clin Exp Allergy. vol. 30. 2000. pp. 1144-50.

Cox, L, Nelson, H, Lockey, R. “Allergen immunotherapy: a practice parameter third update”. J Allergy Clin Immunol. vol. 127. 2011. pp. S1-55.

Bock, SA, Muñoz-Furlong, A, Sampson, HA. “Fatalities due to anaphylactic reactions to foods”. J Allergy Clin Immunol. vol. 107. 2001. pp. 191-3.

Bock, SA, Muñoz-Furlong, A, Sampson, HA. “Further fatalities caused by anaphylactic reactions to food, 2001-2006”. J Allergy Clin Immunol. vol. 119. 2007. pp. 1016-8.

Pumphrey, RS, Gowland, MH. “Further fatal allergic reactions to food in the United Kingdom, 1999-2006”. J Allergy Clin Immunol. vol. 119. 2007. pp. 1018-9.

Greenberger, PA, Rotskoff, BD, Lifschultz, B. “Fatal anaphylaxis: postmortem findings and associated comorbid diseases”. Ann Allergy Asthma Immunol. vol. 98. 2007. pp. 252-7.

Simons, FE, Ardusso, LR, Bilò, MB. “International consensus on (ICON) anaphylaxis”. World Allergy Organ J. vol. 7. 2014. pp. 9.

Muraro, A, Roberts, G, Worm, M. “EAACI Food Allergy and Anaphylaxis Guidelines Group. Anaphylaxis: guidelines from the European Academy of Allergy and Clinical Immunology”. Allergy. vol. 69. 2014. pp. 1026-45.

Wood, RA, Camargo, CA, Lieberman, P. “Anaphylaxis in America: the prevalence and characteristics of anaphylaxis in the United States”. J Allergy Clin Immunol. vol. 133. 2014. pp. 461-7.

Lieberman, P, Nicklas, RA, Randolph, C. “Anaphylaxis–a practice parameter update 2015”. Ann Allergy Asthma Immunol. vol. 115. 2015 Nov. pp. 341-84.

(This practice parameter provides updated guidelines for the diagnosis and management of anaphylaxis using evidence from recent medical literature.)
Simons, FE, Ebisawa, M, Sanchez-Borges, M. “2015 update of the evidence base: World Allergy Organization anaphylaxis guidelines”. World Allergy Organ J. vol. 8. 2015 Oct 28. pp. 32.

(This provides updated evidence supporting recommendations for the diagnosis and management of anaphylaxis.)
Lee, S, Hess, EP, Lohse, C. “Trends, characteristics, and incidence of anaphylaxis in 2001-2010: A population-based study”. J Allergy Clin Immunol. 2016 Jun 4. pp. S0091-6749.

(These data show an increase in the rate of anaphylaxis between 2001-2010 and describe differences in triggers affecting different age groups.)