Child and Chest Health Care Delhi NCR

Assessment of hemodynamic conditions is most important in the management of critically ill patients

It is most important to pick up the condition of compensated shock and start treatment

Pediatric patients go into the stage of decompensated shock a bit late in comparasion to adult patients

Patients are managable in condition of decompesated shock if timely intervention is done.

Once the patient passes into irreversible shock it is very very difficult to revive and mortality is very high

How to recognise a patient clinically in a state of shock

STATE OF STABLE HEMODYNAMICS

Patient has clear consciousness

Periphery is warm and pink

Capillary refill time is 2 seconds or less

Pulse volume is good on palpation

Blood pressure is normal( between 5th to 95th centile for the age

Respiratory rate in the normal range for the age

Heart rate in the normal range for the age

Urine output normal for the age,1ml /kg/hour

STATE OF COMPENSATED SHOCK

Conscioussness inact

Periphery cool

Peripheral pulse ,low volume or thready

Capillary refill time more than 2 seconds

Blood pressure ,systolic is normal but diastolic is in rising trend,postural hypotension,narrow pulse pressure

Heart rate increased for the age

Respiratory rate increased for the age

Urine output reduced

STATE OF DECOMPENSATED SHOCK

Conscioussness-Restlessness or the patient is combative

Periphery on touch is cold and clammy

Capillary refill time is very prolonged like 5 seconds or more with or without mottling of skin

Peripheral pulse is very weak or may not be palpable at all even with great effort

Blood pressure -Hypotension,pulse pressure is 20 mm or less.Blood pressure may not be recordable

Heart rate-increased and in late stage decreased

Respiratory rate-Hyperpnea or Kussmaul breathing pattern(deep and sighy)

Urine output-oliguria or anuria

NORMAL RANGE of Respiratory rate

Premie-40-70/minute

0-3 months-30-60/minute

3-6 months-30-45/minute

6-12 months-25-40/minute

1-3 years-20-30/minute

3-6 years-20-25/minute

6-12 years-14-22/minute

>12 years 12-18/minute

NORMAL RANGE of heart rate- per minute

Premie 120-170

0-3 months 110-160

3-6 months 100-150

6-12 months 90-130

1-3 years 80-125

3-6 years 70-115

6-12 years 60-100

>12 years 60-100

HYPOTENSION is called when systolic blood pressure is below

60mm of Hg in NEW BORN,

70 mm of Hg between the age of 1 month to 1 year

70 mmHg+age in years multiplied by 2 ,between the age of 1- 10 years

90 mm Hg above the age of 10 years

Hypotension is also called when mean arterial pressure (MAP)is below 40+age in years multiplied by 1.5

MANAGEMENT:Management should start at the earliest, at the stage of compensated shock

First attention should be on airway and breathing and oxygen should be given if required to keep SPo2 95% and above

Life saving -for the circulation to be maintained, is fluid therapy

20 ml/kg of N/S or R/L shuold be given over 5-15 minutes and it should be pushed.It can be repeated twice if hydration,circulation and perfusion is not adequate.

In the settings of obvious fluid loss like diarrhoea ,vomiting or hemorrhage ,repeated fluid administration should be done till the signs of fluid overload develop, in the form of tachycardia,bilateral deep inspiratory crackles over subscapular region,liver enlargement,engorgement of jugular vein or signs of pulmonary edema on chest X-Ray

R/L shuold not be used in case of a history of repeated vomiting

IV bolus should be repeated ,only when there is sign of improvement clinically and no sign of fluid overload.

Aggressive fluid therapy may be harmful and should not be given in certain situations like shock in the settings of severe acute malnutrition,severe anemia,compensated shock with high fever with no dehydration or obvious fluid loss(Dengue fever),cardiogenic shock(ductal dependent congenital heart disease in newborn),obstructive shock(tension pneumothorax,cardiac temponade,)

SIGHNS OF CARDIOGENIC SHOCK-Tachycardia,engorged jugular vein,bilateral deep inspiratory crackles over subscapular regions,gallop rhythm,liver enlargement,signs of pulmonary edema on chest X-Ray.

In these cicumstances,crystalloids(N/S or R/L) should be given in the dose of 5-10 ml per kg over 15-30 minutes once then switch over to vasopressors

In case of poor response or no response to fluid therapy,swith over to vasopressures without delay.

If the periphery is cold,give DOPAMINE/EPINEPHRINE

If the perphery is warm give NORADRENALINE

In case of myocardial dysfuntion with maintained blood pressure,give DOBUTAMINE

In case of myocardial dysfuntion with increased peripheral resistance,use MILRINONE

Easy preparation and administration of vasopressures

Dopamine/Dobutamine 6 mg/kg-dilute in 100 ml of D5-1 ml/hour of this will deliver 1 mcg/kg/minute=Dose is 5-20 mcg/kg/minute

EPINEPHRINE0.6mg/kg of body weight,dilute in 100 ml of D5-1ml/hour will deliver 0.1mcg/kg/minute=Dose 0.05 to 0.2mcg/kg/minute,in severe cases upto 1mcg/kg/minute

Norepinephrine 0.6 mg/kg,dilute in 100 ml D5,1ml/hour will deliver 0.1mcg/kg/minute=Dose 0.1-1mcg/kg/hour

REFERENCES1.;Harriet Lane 21 edition

2. CDC guideline on management of shock in children

3.Uptodate-management of shock in children,2021

In the period of october 2021,both Dengue fever and Multi system inflammatory syndrome in children(MIS-C) are being seen in children in Delhi,India

Clinical and laboratory features are overlapping for both these diseases

It is important to differentiate between these as management entirely differs for both

In case of Dengue fever the cornerstone of management is aggressive fluid therapy with crystalloid and colloid with ionotrops if fluid therapy does not work and platelet transfusion if needed.

In cases of MIS-C, the cornerstone of management is steroids and IVIG(Immunoglobulins).Aggressive fluid management may be detrimental in cases of shock with cardiac dysfunction.

Fever are common in both but swellings of feet and hands,diarrhoea,conjuntival injections and altered sensorium along with the laboratory findings of hyperinflammation like highly raised CRP,Leukocytosis,raised D-Dimer are pointers towards MIS-C .In this situations,anti COVID antibody should be done and if positive ,confirms the diagnosis of MIS-C

If fever is associated with vomiting ,erythmatous rashes,myalgia along with the laboratory findings of leucopenia ,severe thrombocytopenia,hemoconcentration , raised serum ferritin level,it points towards the diagnosis of Dengue fever and NS1 antigen and or anti Den IgM should be done which when positive confirms the diagnosis of Dengue fever

In comparision to MIS-C,serum Ferritin level is higher in Dengue fever

References:

1. Ahmed M, Advani S, Moreira A, et al. Multisystem
inflammatory syndrome in children: A systematic review. E
Clin Med. 2020;26:100527.

2.Mishra S, Ramanathan R, Agarwalla SK. Clinical profile of
dengue fever in children: A study from southern Odisha,
India. Scientifica (Cairo). 2016;2016:6391594

3.Indian Pediatrics,volume 58,15 October,2021

Please click below to watch DR.D.K JHA,talking invasive Pediatric Mechanical ventilation in a very simple and enjoying way

• 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.)

Hereditary angioedema is a potential life threatening condition.

It requires earliest possible diagnosis and immediate treatment to save the life in certain cases.

It is caused by either deficiency of C1  inhibitor(Type 1) or dysfunction (Type 2).

It is an autosomal dominant disorder.

In a randomised control trial ,published in JAMA,Lanadelumab,a monoclonal human antibody against Kallikrein was proved to be very effective in reducing the frequency of attacks as well as reducing the severity of individual attack.The level of evidence is level 1,means excellent.

The study was conducted at 41 places in Canada,Jordan,Europe and United states. All the subjects included were previously diagnosed cases of Hereditary angioedema and all were more than 12 years of age.

84 patients were given Lanadelumab and 41 were given placebo.There was a run in period of 4 weeks preceded by 2 weeks of wash out period for any prophylactic treatment being used by patients knowingly or unknowingly. Patients were followed up for a period of 26 weeks for occurence of any episode of angioedema its severity, or any adverse effect of interventional medication.Patients were randomised 2:1 to receive Lanadelumab and placebo. The Lanadelumab receiving patients were divided into 3 groups, and the treatment period was of 26 weeks. The first group received Lanadelumab suncutaneously 150 mg every 4 weeks,second group received 300mg every 4 weeks and the third group 300mg every 2 weeks. The number of episode of angioedema and its severity was observed through a study period of 26 weeks. Adverse events were also observed.

In the group receiving 150mg Lanadelumab subcutaneously every 4 weeks,mean number of attack was 0.48(CI₉₅ 0.31-0.73) in comparision to mean number of attack 1.97 in the placebo group(CI₉₅ 1.64-2.36) ).In the group receiving 300mg of Lanadelumab every 4 weeks .the mean number of attack was 0.5((CI₉₅ 0.36-0.77) ) and for those receiving 300mg of Lanadelumab every 2 weeks the mean number of attack was 0.26(CI₉₅ 0.14-0.46) )

Patients receiving Lanadelumab had improved quality of life with reduced number of attacks(p<0.001),less use of anti C1 inhibitor medications( an20.2% vs 65.9%; p < 0.001) and less episode of moderate to severe attacks(p<0.001)

Adverse effects were seen in 98.5% cases and they were mild to moderate, including headace(7.1%),pain at the site of injection(41.7%),erythma at the site of injection(9.5%) and bruising at the site of injection(6%)

REFERENCES:

Pulmonology Advisor > Trial Tracker > Lanadelumab may be an effective prophylactic treatment for hereditary angioedema

Angioedema is characterised by sudden onset of swelling of eyelids,lips,tounge,genitals,dorsum of the hands and feet,which are visible on clinical examination and not clinically visible swelling of the gastrointestinal tract

Swelling of gastrointestinal tract present as pain abdomen of varying severity .Sometimes, acute severe pain like acute abdomen leading to unnecessary surgery.

Swelling involves the deeper subcutaneous layers.

There may be pain and itching but occasionally only pain is there.

It may take upto 72 hours for the resolution of sewlling.

It may be histamine related or non histamine related.

In histamine related angioedema,urticaria (wheals) will be present along with swelling

There may be a prodrome in the form of tightness or tingling of the area before swelling.

The most serious complication of angioedema is involvement of larynx in the form of laryngeal edema.

When the swelling involves the throat and uvula,it can readily be seen on clinical examination

It  may cause complete obstruction of airway needing intubation and sometimes tracheostomy to save the life.

Fortunately,life threatening episodes are rare.

Dental procedures,with injection of procaine into gum is a common precipitant but laryngeal edema may be spontaneous.

There is no response to epinephrine,antihistamine and corticosteroids on the swelling.

 

If there is only swelling without urticaria,it is not associated with histamine and it may of two types-HEREDITARY AND ACQUIRED ANGIOEDEMA.

HEREDITARY ANGIOEDEMA can be of three types;Type 1-reduced production of C1 inhibitor

Type 2-sufficient production but decreased function of C 1 inhibitor

Type 3-Estrogen dependent,due to mutation in factor xii seen mostly in women

ACQUIRED ANGIOEDEMA can also be of three types;Type 1-associated with reduced C 1esterase inhibitor

Type 2-Drug induced,most common offending drug is ACE inhibitor

Type 3-Histamine dependent regarded as urticaria without wheals

HEREDITARY ANGIOEDEMA is an autosomal dominant disease.

ACQUIRED ANGIOEDEMA may be seen in association with neoplasia,lymphoproliferative disorders and rarely infections.

In case of suspicion of hereditary angioedema type 1 and type 2, decreased levels of serum C 4,C 1inhibitor and decreased function of C 1 inhibitor should be assessed.

TREATMENT

Acute therapy is required during life threatening episodes,which is fortunately rare.

Specific treatment is concentrate of human C1 inhibitor ,the availability of which is limited

The approved drug is BERINERT,used as an intravenous formulation in the dose of 20 unit/kg

In case of non availability of this specific reatment,FFP(fresh frozen plasma) may be used which is least specific but widely available.

Bradykinin type 2 receptor antagonist ICATIBANT is approved for the age of 18 years and older

All treatmens are most effective when they are given early after onset of signs and symptoms

It may take 1-4 hours for the start of action after giving the drug.

Icatibant can be given in ACE inhibitor induced angioedema

Icatibant can be stored on room temperatue and can be given subcutaneously

Icatibant is licensed for home treatment in Europe.

CINRYZE-Purified C1-INH is approved for prophylaxix after acute attack in adolescents and older children

It is given in the dose of 1000 units intravenously twice a week

Danazol is another drug being used as short term prophylaxix ,but it is not given in children,

due to the side effects of premature closure of epiphysis

Danozol increases the production of C1 inhibitor in liver,

For histamine related angioedema, non sedating antihistamine is the drug of choice

In case of no response to usual  dose of nonsedating antihistamine ,the dose may be increased to 4 times

REFERENCES:

• Borzova E and Gratton C ,Angioedema.In Zuberbier Tet al.Urticaria and AngioedemaBerlin:Springer Verlag 2010.122.
• Bindslev-JensenC,CanonicaGV,Church mk,GimenzArnou AM et al. eaaci/ga2lan/edf/wao Guideline .Treatment of Urticaria .Allergy2010;64:1417-1426
• Nelson Textbook of Pediatrics 20 e