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Congential Hypertrophic
pyloric stenosis
PRESENTED BY : DR M.KARTHIK EMMANUEL
MODERATOR: DR P.VENKATESHWARA REDDY
Anatomy of stomach
Introduction
• Male predominance
• Male : female = 5:1
• First born
• Onset of symptoms = 3 – 6 wks after birth
WHY CAN’T SYMPTOMS DEVELOPE AT THE TIME OF BIRTH ????
• Because initially at the time of birth the muscle is looking normal BUT
with time it tends to become hypertrophy and causes obstruction
which leads to symptoms
ASSOCIATED SYNDROMES
• Any congenital or neonatal condition is associated with multiple
syndromes
therefore if we have one anatomical abnormality we should look for
another anatomical abnormality
1. Trisomy 21 & 18
2. Cornelia de lange
3. Apert syndrome ( acrocephalosyndactyly)
4. Paramyotonia congenita
Maternal risk factors
Smoker Obesity
• History of erythromycin intake during pregnancy
• Younger mother ( age <25yrs )
FETAL RISK FACTORS
1. Very preterm
2. First born child
Before knowing the symptoms – lets have a look
on normal physiology of GIT – ESOPHAGUS
• Esophagus = shorter , lower third – peristalsis less efficient
• Regurgitation is common in neonates
HOW TO DIFFERENTIATE WHETHER THE
REGURGITATION IS BECAUSE OF NORMAL PHYSIOLOGY
OR BECAUSE OF CHPS
• Crying increases IAP & makesthe esophagus shorter and incompetent
• Hence this is the reason for regurgitation during crying
SYMPTOMS
• Initially when mother reports they say that the child was regurgitating
• Slowly it turn to vomiting and in turn it becomes projectile
1. Non- bilious projectile vomiting
WHY NON- BILIOUS ????
WHY PROJECTILE ?????
2. Slow weight gain ( weight gain is not good as we expected )
3. After feeding = Characteristic peristaltic wave moving across the
epigastrium noted
EXAMINATION
1. An enlarged pylorus described as olive – palpated in the RUQ or
epigastrium of abdomen in 60 – 80 %
2. Visible persistasis i.e, LUQ to epigastrium = better seen after the
feed
3. Jaundice ( 2% )
WHY JAUNDICE IS SEEN ???
WHY UGT ENZYME IS DOWNREGULATED ??
• We notice decreased hepatic glucuronyl transferase ( liver enzyme )
• Normal function of heptic glucuronyl transferase is – it is the sole
enzyme that can metabolize bilirubin
• Food restriction i.e, starvation appears to selectively downregulate
hepatic UDP-Glucuronyl transferase
HOW TO DIAGNOSE AND CONFIRM ????
1. For diagnosis 3 P’s
• Projectile vomiting
• Peristalsis
• Palpable olive
• Confirmed by USG Abdomen = dignostic if pyloric muscle thickness is
>4mm thickness and muscle length >14mm in term baby
TIMMING OF SURGERY
• It is a MEDICL EMERGENCY ; NOT A SURGICAL EMERGENCY
• Surgery for CHPS is urgent but is not an emergency
• Medical emergency = Dehydration, electrolytes and acid-base
imbalance have to be corrected
Composition of GI secretion
• Stomach has
1. Volume = 1500 ml/24hrs
2. Sodium = 60 mmol/lit ( < plasma level )
3. Pottassium = 10 mmol/lit ( twice the plasma level )
4. Chloride = 130 mmol/lit (> plasma levels )
5. Bicarbonate = zero
• Therefore stomach have much higher concentration of pottassium
and chloride when compared to plasma
Metabolic disturbances
1. Hypovolemia
• Reason: Obstruction – Vomiting of HCL and stomach fluid = first thing we see is
hypovolemia
2 . Metabolic alkalosis
• Reason:1. Obstruction – Vomiting of HCL – Deficiency of H+ & CL- =alkalosis
2. Loss of HCL – less gastric juice entering the duodenum – less pancreatic
HCO3-ion secretion = Hco3 ion retain in the body i.e, persistant metbolic alkalosis
3. Hypo = kalemia,calcemia,natremia
• Reason: As these are the composition of stomach secretions
4. Hypocalcemia ( Reason: Any severe Metabolic alkalosis likely to cause
hypocalcemia )
5. Initially mild cases = Hypo K+,CL- and metabolic alkalosis
severe cases = Progress to metabolic acidosis because of significant
dehydration
NOTE
• Metabolic disturbances varies with depending on the severity of
obstruction
OVERVIEW OF METABOLIC ALKALOSIS + PARADOXICAL ACIDURIA
WHY IT IS CALLED PARADOXICAL ????
WHY ACIDURIA HAPPENING EVEN THOUGH ALKALOSIS EXISTS ??
Arundhati version of CHPS
Body before
Metabolic alkalosis
Metabolicalkalosis
Kidney (RAS) Aldosterone
Kidney coming with Aldosterone
to correct the metabolic
abnormality
With Aldosterone kidney further
worsens the situation i.e,
Met alk + paradoxical aciduria
Body after metabolic abnormality
Kidney inner feeling after worsening the
metabolic abnormality
Actual Rx = I.V fluids Finally I.V fluids ending the
abnormality
• Obstruction – Vomiting of HCL - Deficiency of H+ & CL- = Alkalosis
• Now Renal compensation occurs – Initially Kidney ecretes more
HCO3-ion
• HCO3- ion loss along with NA+ = So urine is rich in HCO3-ion & NA+
• ULTIMA lands in hyponatremia
• Because of which RAS activated – Aldosterone released – acts on
collecting ducts = NA+ and H2O reabsorption and K+,H+ions
excretion
NOTE
1. Inspite of body having metabolic alkalosis – body tends to cause
aciduria which is a paradox ( normally body should excrete HCO3-
ion as a compensatory mechanism )
NORMAL PHYSIOLOGY
• In adults – ICF is much higher than ECF volume
• In neonates – ECF is higher than ICF
• These implies – DEHYDRATION can occurs quickly and they also have
higher body water turn over. So they tends to loose around 30 – 40%
of body fluid through urine,feces sweating & respiration
Response to metabolic alkalosis
• Respiratory response – Hypoventilation which causes Respiratory acidosis
SIGNS OF DEHYDRATION
1. Sunken eyes
2. Sunken anterior fontanella ( Normally closes @ 12-18 months )
3. Prolonged CRT i.e, > 2sec ( Normally < 2sec )
4. Decreased skin turgor
5. Weight change
6. Normally diapers are wet every 3 – 4hrs but in these we see dry diapers
CLINICAL SIGNIFICANCE OF HYPOCALCEMIA
• Neonates tends to have calcium dependant myocardial contractility
• Therefore hypocalcemia- Decreases cardiac contractility which further
decreases cardiac output
NORMAL PHYSIOLOGY OF CARDIAC OUTPUT
1. CARDIAC OUTPUT
• Because of higher metabolism in children,they tends to have
higher cardiac output (Neonates = 300 – 400ml/kg/min ;
Adult = 100ml/kg/min )
HEART RATE DEPENDENT CARDIAC OUTPUT - REASON
??????
• Cannot increase the myocardial contractility to an extent that they can
increase the CO. So any increase in CO depends on HR
• Childrens already have higher baseline HR, even this capacity to increase
the CO is limited in smaller children & neonate
WHY DO THEY HAVE DECREASED MYOCARDIAL
CONTRACTILITY ???????
• Disorganised myofibrils, immature sarcoplasmic reticulum & immature T-
tubules
• Actual myocardium contains fibers – amount of muscle in fibers is less,they
have more collagen content = bcz of which the tension developed in the
cardiac muscle at EDV is much less it means the SV also compromised
Calcium sensitive myocardial contractility
• Normally calcium levels influence cardiac contractility
• Anything which decreases serum calcium levels i.e, rapid blood
transfusions, calcium channel blockers, severe metabolic alkalosis
decreases myocardial contractility
NOTE
• In metabolic alkalosis, bound hydrogen ions dissociate from albumin
which increases the fraction of albumin available for ionized calcium
binding
• Therefoere metabolic alkalosis leads to hypocalcemia
Before going to treatment part – lets have a
look on normal physiology
RENAL
• Neonates have lower RBF, lower GFR, lower tubular
function
• These manifested as
1. Drugs excretion can be delayed
2. Fluids,electrolytes and acid base homeostasis may
be impaired in infants ( as kidney is responsible for
fluids, electrolytes, acid base homeostasis)
NOTE
• They are more prone for fluid overload or dehydration if we don’t
manage them adequately
GLUCOSE HOMEOSTASIS – LIVER
Why HYPOGLYCEMIA is more common in preterm
&neonates???
• Childrens tends to have low or No glycogen reserve in the liver
• Therefore need dextrose 10% infusion = 3 – 5ml/kg/hr
intraoperatively
• Symptoms of hypoglycemia =jitteriness, convulsions and apnea
HYPERGLYCEMIA
• Because the kidneys cannot necessarily reabsorb the excess glucose,if
we give too much glucose to the small child it causes
1. Osmotic diuresis
2. Osmotically induced cerebral fluid shifts may leads to cerebral
haemorrhage
3. Glycosuria
4. Increased extent of neurologic damage during a cerebral hypoxic
ischemic event
TREATMENT WITH INTRAVENOUS FLUIDS
1. NPO ( As already vomiting symptom present )
2. Sodium , Dextrose , Pottassium ( Re-establish the volume status
along with electrolytes status )
3. Start Pottassium supplementation ONLY after the neonate start
producing urine –
WHY WE HAVE TO START K+ ONLY AFTER PRODUCING URINE ??????
• Once we correct hypovolemia with 0.9%NS boluses – make sure that
the child is passing urine then only start K+ with maintenance fluids
because pottassium has to be excreted in urine
FLUID MANAGEMENT
1. Correct hypovolemia
• 0.9% NS in boluses of 10ml/kg
2. Replace NG losses
• 1ml of gastric losses must be replaced with 1ml of 0.9% NS + 10mmol
of KCL per 500ml bag
3. Maintenance
• HCO3 if >25mmol/lit = DNS + 10mmol KCL per 500ml bag @
150ml/kg/day
• HCO3 if <25mmol/lit = DNS + 10mmol KCL per 500ml bag @
100ml/kg/day
• Infants < 44 post conceptual weeks = has poor glycogen stores in
liver,therefore supplement 10% dextrose if they are NPO
WHY SMALL CHILD CAN’T TOLERATE TOO MUCH
FLUIDS NOR TOO MUCH SYSTEMIC VASCULAR
RESISTANCE ????
• Myocardial contractile reserve is low ( Preload and
after load tolerance is poor ). All these compromises
the CO which decreases the SV
AIM OF OPTIMIZATION FOR TAKING UP FOR SURGERY
1. Chloride > 100meq/lit
2. HCO3 < 30meq/lit ( To avoid to much of alkalosis )
3. Urine output > 1 – 2ml/kg/hr
4. Pottassium > 3meq/lit
5. Sodium > 130meq/lit
WHY ALKALOSIS CORRECTION IS SO
IMPORTANT ??????
• Normally H+ions will go and stimulate respiratory center
• Therefore persistent alkalosis can depress the respiratory drive, thus
risk for post operative apnea
WHAT ARE THE THINGS TO BE DONE PRIOR TO INDUCTION ??
• Good intravenous access , volume status
• Suction – to make sure that the stomach is empty
• Some times they rotate the child until minimum to no gastric
contents return
INDUCTION
1. Classic RSI – Predetermined dose of induction agent + muscle
relaxant (sch) – wait for 60sec & then intubate
• But in paediatric age group especially neonates – Apnea tolerance is
limited which means they can’t tolerate the 60sec apnea time
WHY APNEA TOLERANCE IS LIMITED OR WHY THEY ARE
VULNERABLE TO HYPOXIA ??????
1. Low FRC
• FRC indicates oxygen reserve we have during the apneic
period
• It is the balance between the compliance of chest wall &
lung
• In children chest wall compliance is 3 – 6 times more
compliant than the lung compliance
• Therefore FRC is on lower end. So, during normal respiration
significant percent of the alveoli will be closed in children. So they are
more susceptible to hypoxia when they have apneic episodes
COMPENSATION FOR LOW FRC
• Laryngeal braking- partial adduction of vocal cords during
expiration which is seen clinically as grunting ( Normally
GRUNTING indicate respiratory pathology but in children it is
a normal phenomenon to compensate for low FRC )
• Increased RR – decreases the duration of inspiration &
expiration – tends to create Intrinsic PEEP which increases
FRC
• Narrow nasal passage offers resistance to expiratory flow
2. High oxygen consumption
• Childrens tends to have faster metabolism
• Higher work of breathing ( accounts for 15% of O2 consumption)
3. Higher airway resistance
4. Compliant chest wall
2.Because of all the above things we go for MODIFIED RSI
• Induction + sch = once after giving sch,do gentle mask ventilation for
30 – 40sec then intubate. This minimizes the possibility of
desaturation & give time to intubation as well
3. Awake intubation is avoid bcz of risk of intraventricular
haemorrhage
SURGERY
• Ramstedt pyloromyotomy
• Duration of surgery = 30mins
• Can be open or laproscopic
Disadvantage of laproscopy
1. Increased incidence of inadequate pyloromyotomy
2. Increased risk of mucosal perforation in the pyloric canal & of tear
of duodenal cap – bcz they tend to elevate the duodenum & do
splitting
Advantage of laproscopy – feeding can be started even more earlier
when compare to open
• Incisions – Right hypochondrium incision or periumbilical incision
Steps of surgery
1. After incision – pulling of pylorus out
2. Split the pylorus open
3. Once if we see the lining of pylorus bulging out of incision it indicates
that the surgery is successful i.e, we have split the hypertrophic muscle
completely
NOTE
• After opening the pylorus muscle some surgeons may ask for air inje tion of
50 – 100ml into NG tube to verify the integrity of duodenal mucosa
• If there is no bubbling air through mucosa indicates no leak
• Make sure that after checking – aspirate the air back again
ANALGESIA
• Generally postoperative pain in this surgery is minimally noted
• PCM
• Wound infiltration
• Opioids – best avoided – reason ????
1. Because of immature hepatic system opioid metabolism is slow
2. Because of potential for alkalosis- increased Sn to opioids noted
which results in decreased respiratory drive
POSTOPERATIVE COMPLCATIONS
1. Presence of metabolic alkalosis increases the risk of apnea
2. Perforation of stomach – leakage – sepsis
3. Persistent vomiting – Inadequate division of hypertrophic muscle
• Feeding – start few hours after surgery
SUMMARY
1. It is a medical emergency
2. Correction of acid-base, electrolyte & volume repletion
3. Target preoperative = Hco3 < 30meq/lit
4. Surgery - short duration, less painful & good recovery
CONGENITAL HYPERTROPHIC PYLORIC STENOSIS  by Dr M.KARTHIK EMMANUEL

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CONGENITAL HYPERTROPHIC PYLORIC STENOSIS by Dr M.KARTHIK EMMANUEL

  • 1. Congential Hypertrophic pyloric stenosis PRESENTED BY : DR M.KARTHIK EMMANUEL MODERATOR: DR P.VENKATESHWARA REDDY
  • 3. Introduction • Male predominance • Male : female = 5:1 • First born • Onset of symptoms = 3 – 6 wks after birth WHY CAN’T SYMPTOMS DEVELOPE AT THE TIME OF BIRTH ????
  • 4. • Because initially at the time of birth the muscle is looking normal BUT with time it tends to become hypertrophy and causes obstruction which leads to symptoms ASSOCIATED SYNDROMES • Any congenital or neonatal condition is associated with multiple syndromes therefore if we have one anatomical abnormality we should look for another anatomical abnormality 1. Trisomy 21 & 18 2. Cornelia de lange 3. Apert syndrome ( acrocephalosyndactyly) 4. Paramyotonia congenita
  • 6. • History of erythromycin intake during pregnancy • Younger mother ( age <25yrs ) FETAL RISK FACTORS 1. Very preterm 2. First born child
  • 7. Before knowing the symptoms – lets have a look on normal physiology of GIT – ESOPHAGUS • Esophagus = shorter , lower third – peristalsis less efficient • Regurgitation is common in neonates HOW TO DIFFERENTIATE WHETHER THE REGURGITATION IS BECAUSE OF NORMAL PHYSIOLOGY OR BECAUSE OF CHPS • Crying increases IAP & makesthe esophagus shorter and incompetent • Hence this is the reason for regurgitation during crying
  • 8. SYMPTOMS • Initially when mother reports they say that the child was regurgitating • Slowly it turn to vomiting and in turn it becomes projectile 1. Non- bilious projectile vomiting WHY NON- BILIOUS ???? WHY PROJECTILE ????? 2. Slow weight gain ( weight gain is not good as we expected ) 3. After feeding = Characteristic peristaltic wave moving across the epigastrium noted
  • 9.
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  • 11. EXAMINATION 1. An enlarged pylorus described as olive – palpated in the RUQ or epigastrium of abdomen in 60 – 80 % 2. Visible persistasis i.e, LUQ to epigastrium = better seen after the feed 3. Jaundice ( 2% ) WHY JAUNDICE IS SEEN ??? WHY UGT ENZYME IS DOWNREGULATED ??
  • 12. • We notice decreased hepatic glucuronyl transferase ( liver enzyme ) • Normal function of heptic glucuronyl transferase is – it is the sole enzyme that can metabolize bilirubin • Food restriction i.e, starvation appears to selectively downregulate hepatic UDP-Glucuronyl transferase HOW TO DIAGNOSE AND CONFIRM ???? 1. For diagnosis 3 P’s • Projectile vomiting • Peristalsis • Palpable olive
  • 13. • Confirmed by USG Abdomen = dignostic if pyloric muscle thickness is >4mm thickness and muscle length >14mm in term baby TIMMING OF SURGERY • It is a MEDICL EMERGENCY ; NOT A SURGICAL EMERGENCY • Surgery for CHPS is urgent but is not an emergency • Medical emergency = Dehydration, electrolytes and acid-base imbalance have to be corrected
  • 14. Composition of GI secretion • Stomach has 1. Volume = 1500 ml/24hrs 2. Sodium = 60 mmol/lit ( < plasma level ) 3. Pottassium = 10 mmol/lit ( twice the plasma level ) 4. Chloride = 130 mmol/lit (> plasma levels ) 5. Bicarbonate = zero • Therefore stomach have much higher concentration of pottassium and chloride when compared to plasma
  • 15. Metabolic disturbances 1. Hypovolemia • Reason: Obstruction – Vomiting of HCL and stomach fluid = first thing we see is hypovolemia 2 . Metabolic alkalosis • Reason:1. Obstruction – Vomiting of HCL – Deficiency of H+ & CL- =alkalosis 2. Loss of HCL – less gastric juice entering the duodenum – less pancreatic HCO3-ion secretion = Hco3 ion retain in the body i.e, persistant metbolic alkalosis 3. Hypo = kalemia,calcemia,natremia • Reason: As these are the composition of stomach secretions 4. Hypocalcemia ( Reason: Any severe Metabolic alkalosis likely to cause hypocalcemia )
  • 16. 5. Initially mild cases = Hypo K+,CL- and metabolic alkalosis severe cases = Progress to metabolic acidosis because of significant dehydration NOTE • Metabolic disturbances varies with depending on the severity of obstruction OVERVIEW OF METABOLIC ALKALOSIS + PARADOXICAL ACIDURIA WHY IT IS CALLED PARADOXICAL ???? WHY ACIDURIA HAPPENING EVEN THOUGH ALKALOSIS EXISTS ??
  • 20. Kidney coming with Aldosterone to correct the metabolic abnormality With Aldosterone kidney further worsens the situation i.e, Met alk + paradoxical aciduria
  • 21. Body after metabolic abnormality
  • 22. Kidney inner feeling after worsening the metabolic abnormality
  • 23. Actual Rx = I.V fluids Finally I.V fluids ending the abnormality
  • 24. • Obstruction – Vomiting of HCL - Deficiency of H+ & CL- = Alkalosis • Now Renal compensation occurs – Initially Kidney ecretes more HCO3-ion • HCO3- ion loss along with NA+ = So urine is rich in HCO3-ion & NA+ • ULTIMA lands in hyponatremia • Because of which RAS activated – Aldosterone released – acts on collecting ducts = NA+ and H2O reabsorption and K+,H+ions excretion NOTE 1. Inspite of body having metabolic alkalosis – body tends to cause aciduria which is a paradox ( normally body should excrete HCO3- ion as a compensatory mechanism )
  • 26. • In adults – ICF is much higher than ECF volume • In neonates – ECF is higher than ICF • These implies – DEHYDRATION can occurs quickly and they also have higher body water turn over. So they tends to loose around 30 – 40% of body fluid through urine,feces sweating & respiration
  • 27. Response to metabolic alkalosis • Respiratory response – Hypoventilation which causes Respiratory acidosis SIGNS OF DEHYDRATION 1. Sunken eyes 2. Sunken anterior fontanella ( Normally closes @ 12-18 months ) 3. Prolonged CRT i.e, > 2sec ( Normally < 2sec ) 4. Decreased skin turgor 5. Weight change 6. Normally diapers are wet every 3 – 4hrs but in these we see dry diapers
  • 28. CLINICAL SIGNIFICANCE OF HYPOCALCEMIA • Neonates tends to have calcium dependant myocardial contractility • Therefore hypocalcemia- Decreases cardiac contractility which further decreases cardiac output NORMAL PHYSIOLOGY OF CARDIAC OUTPUT 1. CARDIAC OUTPUT • Because of higher metabolism in children,they tends to have higher cardiac output (Neonates = 300 – 400ml/kg/min ; Adult = 100ml/kg/min )
  • 29. HEART RATE DEPENDENT CARDIAC OUTPUT - REASON ?????? • Cannot increase the myocardial contractility to an extent that they can increase the CO. So any increase in CO depends on HR • Childrens already have higher baseline HR, even this capacity to increase the CO is limited in smaller children & neonate WHY DO THEY HAVE DECREASED MYOCARDIAL CONTRACTILITY ??????? • Disorganised myofibrils, immature sarcoplasmic reticulum & immature T- tubules • Actual myocardium contains fibers – amount of muscle in fibers is less,they have more collagen content = bcz of which the tension developed in the cardiac muscle at EDV is much less it means the SV also compromised
  • 30. Calcium sensitive myocardial contractility • Normally calcium levels influence cardiac contractility • Anything which decreases serum calcium levels i.e, rapid blood transfusions, calcium channel blockers, severe metabolic alkalosis decreases myocardial contractility NOTE • In metabolic alkalosis, bound hydrogen ions dissociate from albumin which increases the fraction of albumin available for ionized calcium binding • Therefoere metabolic alkalosis leads to hypocalcemia
  • 31. Before going to treatment part – lets have a look on normal physiology RENAL • Neonates have lower RBF, lower GFR, lower tubular function • These manifested as 1. Drugs excretion can be delayed 2. Fluids,electrolytes and acid base homeostasis may be impaired in infants ( as kidney is responsible for fluids, electrolytes, acid base homeostasis)
  • 32. NOTE • They are more prone for fluid overload or dehydration if we don’t manage them adequately GLUCOSE HOMEOSTASIS – LIVER Why HYPOGLYCEMIA is more common in preterm &neonates??? • Childrens tends to have low or No glycogen reserve in the liver • Therefore need dextrose 10% infusion = 3 – 5ml/kg/hr intraoperatively • Symptoms of hypoglycemia =jitteriness, convulsions and apnea
  • 33. HYPERGLYCEMIA • Because the kidneys cannot necessarily reabsorb the excess glucose,if we give too much glucose to the small child it causes 1. Osmotic diuresis 2. Osmotically induced cerebral fluid shifts may leads to cerebral haemorrhage 3. Glycosuria 4. Increased extent of neurologic damage during a cerebral hypoxic ischemic event
  • 34. TREATMENT WITH INTRAVENOUS FLUIDS 1. NPO ( As already vomiting symptom present ) 2. Sodium , Dextrose , Pottassium ( Re-establish the volume status along with electrolytes status ) 3. Start Pottassium supplementation ONLY after the neonate start producing urine – WHY WE HAVE TO START K+ ONLY AFTER PRODUCING URINE ??????
  • 35. • Once we correct hypovolemia with 0.9%NS boluses – make sure that the child is passing urine then only start K+ with maintenance fluids because pottassium has to be excreted in urine FLUID MANAGEMENT 1. Correct hypovolemia • 0.9% NS in boluses of 10ml/kg 2. Replace NG losses • 1ml of gastric losses must be replaced with 1ml of 0.9% NS + 10mmol of KCL per 500ml bag 3. Maintenance • HCO3 if >25mmol/lit = DNS + 10mmol KCL per 500ml bag @ 150ml/kg/day
  • 36. • HCO3 if <25mmol/lit = DNS + 10mmol KCL per 500ml bag @ 100ml/kg/day • Infants < 44 post conceptual weeks = has poor glycogen stores in liver,therefore supplement 10% dextrose if they are NPO WHY SMALL CHILD CAN’T TOLERATE TOO MUCH FLUIDS NOR TOO MUCH SYSTEMIC VASCULAR RESISTANCE ???? • Myocardial contractile reserve is low ( Preload and after load tolerance is poor ). All these compromises the CO which decreases the SV
  • 37. AIM OF OPTIMIZATION FOR TAKING UP FOR SURGERY 1. Chloride > 100meq/lit 2. HCO3 < 30meq/lit ( To avoid to much of alkalosis ) 3. Urine output > 1 – 2ml/kg/hr 4. Pottassium > 3meq/lit 5. Sodium > 130meq/lit
  • 38. WHY ALKALOSIS CORRECTION IS SO IMPORTANT ??????
  • 39. • Normally H+ions will go and stimulate respiratory center • Therefore persistent alkalosis can depress the respiratory drive, thus risk for post operative apnea WHAT ARE THE THINGS TO BE DONE PRIOR TO INDUCTION ?? • Good intravenous access , volume status • Suction – to make sure that the stomach is empty • Some times they rotate the child until minimum to no gastric contents return INDUCTION 1. Classic RSI – Predetermined dose of induction agent + muscle relaxant (sch) – wait for 60sec & then intubate
  • 40. • But in paediatric age group especially neonates – Apnea tolerance is limited which means they can’t tolerate the 60sec apnea time WHY APNEA TOLERANCE IS LIMITED OR WHY THEY ARE VULNERABLE TO HYPOXIA ?????? 1. Low FRC • FRC indicates oxygen reserve we have during the apneic period • It is the balance between the compliance of chest wall & lung • In children chest wall compliance is 3 – 6 times more compliant than the lung compliance
  • 41. • Therefore FRC is on lower end. So, during normal respiration significant percent of the alveoli will be closed in children. So they are more susceptible to hypoxia when they have apneic episodes COMPENSATION FOR LOW FRC • Laryngeal braking- partial adduction of vocal cords during expiration which is seen clinically as grunting ( Normally GRUNTING indicate respiratory pathology but in children it is a normal phenomenon to compensate for low FRC ) • Increased RR – decreases the duration of inspiration & expiration – tends to create Intrinsic PEEP which increases FRC • Narrow nasal passage offers resistance to expiratory flow
  • 42. 2. High oxygen consumption • Childrens tends to have faster metabolism • Higher work of breathing ( accounts for 15% of O2 consumption) 3. Higher airway resistance 4. Compliant chest wall 2.Because of all the above things we go for MODIFIED RSI • Induction + sch = once after giving sch,do gentle mask ventilation for 30 – 40sec then intubate. This minimizes the possibility of desaturation & give time to intubation as well 3. Awake intubation is avoid bcz of risk of intraventricular haemorrhage
  • 43. SURGERY • Ramstedt pyloromyotomy • Duration of surgery = 30mins • Can be open or laproscopic Disadvantage of laproscopy 1. Increased incidence of inadequate pyloromyotomy 2. Increased risk of mucosal perforation in the pyloric canal & of tear of duodenal cap – bcz they tend to elevate the duodenum & do splitting Advantage of laproscopy – feeding can be started even more earlier when compare to open
  • 44. • Incisions – Right hypochondrium incision or periumbilical incision Steps of surgery 1. After incision – pulling of pylorus out 2. Split the pylorus open 3. Once if we see the lining of pylorus bulging out of incision it indicates that the surgery is successful i.e, we have split the hypertrophic muscle completely NOTE • After opening the pylorus muscle some surgeons may ask for air inje tion of 50 – 100ml into NG tube to verify the integrity of duodenal mucosa • If there is no bubbling air through mucosa indicates no leak • Make sure that after checking – aspirate the air back again
  • 45. ANALGESIA • Generally postoperative pain in this surgery is minimally noted • PCM • Wound infiltration • Opioids – best avoided – reason ???? 1. Because of immature hepatic system opioid metabolism is slow 2. Because of potential for alkalosis- increased Sn to opioids noted which results in decreased respiratory drive POSTOPERATIVE COMPLCATIONS 1. Presence of metabolic alkalosis increases the risk of apnea 2. Perforation of stomach – leakage – sepsis 3. Persistent vomiting – Inadequate division of hypertrophic muscle
  • 46. • Feeding – start few hours after surgery SUMMARY 1. It is a medical emergency 2. Correction of acid-base, electrolyte & volume repletion 3. Target preoperative = Hco3 < 30meq/lit 4. Surgery - short duration, less painful & good recovery