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case discussion

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  • vivek gupta
    i was out on td and conference regarding case on DKA FEW POINTS 1. tachycardia could be because of compensated shock , sepsis and stress however no where
    Message 1 of 8 , Mar 6, 2011
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      i was out on td and conference regarding case on DKA
      FEW POINTS
      1. tachycardia could be because of  compensated shock , sepsis and stress however no where initial BP/CFT is mentioned. if child was in shock initially 10ml/kg boluses should have been repeated till circulation restored and not given over 12 hour as 40 ml/kg scattered.
      2. blood sugar was allowed to fall less than 100 and at 75 10 % dex was added. as per guidelines sugar <150 10 % dex should be added or we can reduced the insulin rate.even one blood sugar reading is 54.
      3. dopamine was required because probably we could have give him soadabicarb recommendation ph <6.9 or even < 7. in shock and acidosis dopamine wont work and and shock will worsen so will the tachycardia.
      4. 10 % dex was changed to 7.5% at 101 which lead to a dip to 54. i think we could have continued with 10 % dex. too much fluctuation in milieu is detrimental.

      all said and done its easier to be wiser retrospectively . 

      SQN LDR VIVEK KUMAR MD DNB
      GRADED SPECIALIST PEDIATRICS 12 AFH GORAKHPUR


    • biju john
      I have the following to submit: (i) Management of DKA and hypovolemia is different form any other similar setting.Every case of DKA will come to us with
      Message 2 of 8 , Mar 6, 2011
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        I have the following to submit:
        (i) Management of DKA and hypovolemia is different form any other similar setting.Every case of DKA will come to us with dehydration ,the assessment of extent of which is rather difficult.
        (ii)One could pick up any current protocol to see the differences(references below)
        (iii)I reiterate,avoid too many boluses and bicarbonate.

        (From Australian guidelines)-Quote-

        "AIMS OF TREATMENT PAEDIATRIC vs ADULT

        The aims of treatment of DKA are different for paediatrics and adults.

        Children are at high risk of cerebral oedema but they tolerate hypovolaemia well.

        Adults tolerate hypovolaemia poorly and are at low risk of cerebral oedema.

        Hence the aims of treatment of DKA for:

        Paediatrics is to achieve perfusion to avoid acute tubular necrosis but keep them relatively dehydrated while the metabolic defect is corrected.

        Adults is to correct hypovolaemia and the metabolic defect.

        Fluid therapy in paediatrics aims to correct the fluid deficit over 48 hours while in adults the fluid deficit is replaced in 24 hours or less.
         

        1.BSPED Recommended DKA Guidelines 2009

        2.ISPAD Clinical Practice Consensus Guidelines 2009 Compendium.

        .Diabetic ketoacidosis in children and adolescents with diabetes
        3.Diabetic ketoacidosis.
        Current Paediatrics (2006)
        16, 111116

        4.Diabetic Ketoacidosis in Infants, Children, and Adolescents.

        A consensus statement from the American Diabetes Association 2006

        5.DKA in Pediatric critical care.Fuhrman and Zimmerman

         

        By next edition ,Either Nelson will change its stand on Milwaukee protocol or all these protocols from different countries will change based on available evidence at that time.Till then we shall follow what is  'currently available evidence based medicine'

         

        Regards,

        Wg Cdr B M John

         

         



        --- On Sun, 3/6/11, vivek gupta <vkg3679@...> wrote:

        From: vivek gupta <vkg3679@...>
        Subject: [defencepeds] case discussion
        To: defencepeds@yahoogroups.com
        Date: Sunday, March 6, 2011, 4:09 PM

         
        i was out on td and conference regarding case on DKA
        FEW POINTS
        1. tachycardia could be because of  compensated shock , sepsis and stress however no where initial BP/CFT is mentioned. if child was in shock initially 10ml/kg boluses should have been repeated till circulation restored and not given over 12 hour as 40 ml/kg scattered.
        2. blood sugar was allowed to fall less than 100 and at 75 10 % dex was added. as per guidelines sugar <150 10 % dex should be added or we can reduced the insulin rate.even one blood sugar reading is 54.
        3. dopamine was required because probably we could have give him soadabicarb recommendation ph <6.9 or even < 7. in shock and acidosis dopamine wont work and and shock will worsen so will the tachycardia.
        4. 10 % dex was changed to 7.5% at 101 which lead to a dip to 54. i think we could have continued with 10 % dex. too much fluctuation in milieu is detrimental.

        all said and done its easier to be wiser retrospectively . 

        SQN LDR VIVEK KUMAR MD DNB
        GRADED SPECIALIST PEDIATRICS 12 AFH GORAKHPUR



      • rakhee.garg
        Respected Seniors and Colleagues I would like to share my recent experience of managing a neonate.Comments are invited. case summary 20 days old neonate a
        Message 3 of 8 , Mar 16, 2012
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          Respected Seniors and Colleagues
          I would like to share my recent experience of managing a neonate.Comments are invited.

          case summary

          20 days old neonate a product of non-consanguineous marriage admitted to our hospital with h/o fever, high grade, intermittent, not feeding well, vomiting and lethargic. On examination HR 176/min, RR 64/min, temp 100 F, SPO2 98%, CFT <3sec, wt 3.8kg (B. WT 3.2Kg) pallor +ve, abdomen was distended, liver palpable 3cm below rt costal margin, spleen tip palpable On investigation Hb 8.6gm%, TLC 4000, Neutrophil 33%, lymphocyte 62%, platelet 1lac, CRP 60 and PBS S/O sepsis, CXR and Transcranial USG were WNL. Baby was started on broad spectrum antibiotic. After 48hrs of antibiotic, child responded partially but still fever persisting . Card test for MP and PBS for MP was sent and found to be positive for plasmodium Vivax. Baby was started on chloroquine, baby responded to treatment. Incidentally while dispatching the blood sample in plain sterile vacutainer, sample was found to be chylous . Our laboratory reported sample chylous in appearance, total cholesterol 220 mg/dl, Tgs 2039mg/dl, direct HDL 15mg/dl and LDL 107mg/dl. Test repeated by spectrometry and electrophoresis cholesterol 202 mg/dl, Triglycerides 1588 mg/dl, HDL 30.46 mg/dl, LDL 97.75 mg/dl, VLDL 73.79 mg/dL, Chylomicron nil , thyroid profile , BSL , S. Amylase,S. albumin were wnl. USG abdomen was s/o of hepatosplenomegaly with no feature s/o pancreatitis. There were no eruptive xanthomas, fundus examination was normal. Baby was born to 24 yrs old booked and immunized primigravida at term with birth wt 3.2kg. Perinatal period was uneventful. No family history of dyslipidaemia. Lipid profiles of mother shows mild increase in triglyceride level otherwise lipid profile of both parents were essentially normal. Child was diagnosed as a case of familial hypertriglyceridaemia (FHTG). Baby was managed with low fat milk, vit ADEK ,carnitine supplement and MCT oil. On follow up baby is thriving well and lipid profile achieved near normal over 1month on low fat milk, mct oil and fat soluble vit.Presently father is posted out to pathankot,hope parent has reported to maj Rahul for follow up.

          Neonatal hypertriglyceridaemia is extremely rare characterized by moderately elevated plasma triglyceride accompanied by modest elevations in cholesterol. VLDL is the major class of lipoproteins elevated in this disorder, which is referred to as type four hyperlipoproteinemia. The diagnosis of FHTG is suggested in our case by elevated plasma triglycerides 1588 mg/dl (30-86), VLDL 73.79 mg/dl (20-40), mildly elevated cholesterol 202 mg/dl (45-182) with normal HDL 30.46 mg/dl (30-70), LDL 97.75 mg/dl and Chylomicron. Secondary causes ruled out by normal blood sugar level, thyroid profile, LFT, RFT and no history of any drug intake except chloroquine, ceftriazone and amikacin. But there was similar case reported by MS Tullu etal in eight-month-old boy admitted for malaria and anemia, incidentally diagnosed as a case of FHTG due to lipemic serum .He had elevated serum triglycerides with normal serum cholesterol, but had no symptoms related to the primary disorder (FHTG). There is no case report/literature suggesting association of malaria with hypertriglyceridaemia. There are few case report of type 1 and type V hypertriglyceridaemia in neonatal period . But no case report or literature found suggesting type IV FHTG with such high level of triglyceride with normal chylomicron level in neonate.


          with warm regards
          Sqn Ldr AK Garg
          Gd splt paed,7 Air Force Hosp,Kanpur
        • DALJIT SINGH
          Dear Sqn Ldr Garg, You must publish this case. Daljit
          Message 4 of 8 , Mar 17, 2012
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            Dear Sqn Ldr Garg,
            You must publish this case.
            Daljit

            On 3/16/12, rakhee.garg <rakhee.garg@...> wrote:
            > Respected Seniors and Colleagues
            > I would like to share my recent experience of managing a neonate.Comments
            > are invited.
            >
            > case summary
            >
            > 20 days old neonate a product of non-consanguineous marriage admitted to our
            > hospital with h/o fever, high grade, intermittent, not feeding well,
            > vomiting and lethargic. On examination HR 176/min, RR 64/min, temp 100 F,
            > SPO2 98%, CFT <3sec, wt 3.8kg (B. WT 3.2Kg) pallor +ve, abdomen was
            > distended, liver palpable 3cm below rt costal margin, spleen tip palpable
            > On investigation Hb 8.6gm%, TLC 4000, Neutrophil 33%, lymphocyte 62%,
            > platelet 1lac, CRP 60 and PBS S/O sepsis, CXR and Transcranial USG were WNL.
            > Baby was started on broad spectrum antibiotic. After 48hrs of antibiotic,
            > child responded partially but still fever persisting . Card test for MP and
            > PBS for MP was sent and found to be positive for plasmodium Vivax. Baby was
            > started on chloroquine, baby responded to treatment. Incidentally while
            > dispatching the blood sample in plain sterile vacutainer, sample was found
            > to be chylous . Our laboratory reported sample chylous in appearance, total
            > cholesterol 220 mg/dl, Tgs 2039mg/dl, direct HDL 15mg/dl and LDL 107mg/dl.
            > Test repeated by spectrometry and electrophoresis cholesterol 202 mg/dl,
            > Triglycerides 1588 mg/dl, HDL 30.46 mg/dl, LDL 97.75 mg/dl, VLDL 73.79
            > mg/dL, Chylomicron nil , thyroid profile , BSL , S. Amylase,S. albumin
            > were wnl. USG abdomen was s/o of hepatosplenomegaly with no feature s/o
            > pancreatitis. There were no eruptive xanthomas, fundus examination was
            > normal. Baby was born to 24 yrs old booked and immunized primigravida at
            > term with birth wt 3.2kg. Perinatal period was uneventful. No family history
            > of dyslipidaemia. Lipid profiles of mother shows mild increase in
            > triglyceride level otherwise lipid profile of both parents were essentially
            > normal. Child was diagnosed as a case of familial hypertriglyceridaemia
            > (FHTG). Baby was managed with low fat milk, vit ADEK ,carnitine supplement
            > and MCT oil. On follow up baby is thriving well and lipid profile achieved
            > near normal over 1month on low fat milk, mct oil and fat soluble
            > vit.Presently father is posted out to pathankot,hope parent has reported to
            > maj Rahul for follow up.
            >
            > Neonatal hypertriglyceridaemia is extremely rare characterized by moderately
            > elevated plasma triglyceride accompanied by modest elevations in
            > cholesterol. VLDL is the major class of lipoproteins elevated in this
            > disorder, which is referred to as type four hyperlipoproteinemia. The
            > diagnosis of FHTG is suggested in our case by elevated plasma triglycerides
            > 1588 mg/dl (30-86), VLDL 73.79 mg/dl (20-40), mildly elevated cholesterol
            > 202 mg/dl (45-182) with normal HDL 30.46 mg/dl (30-70), LDL 97.75 mg/dl and
            > Chylomicron. Secondary causes ruled out by normal blood sugar level,
            > thyroid profile, LFT, RFT and no history of any drug intake except
            > chloroquine, ceftriazone and amikacin. But there was similar case reported
            > by MS Tullu etal in eight-month-old boy admitted for malaria and anemia,
            > incidentally diagnosed as a case of FHTG due to lipemic serum .He had
            > elevated serum triglycerides with normal serum cholesterol, but had no
            > symptoms related to the primary disorder (FHTG). There is no case
            > report/literature suggesting association of malaria with
            > hypertriglyceridaemia. There are few case report of type 1 and type V
            > hypertriglyceridaemia in neonatal period . But no case report or literature
            > found suggesting type IV FHTG with such high level of triglyceride with
            > normal chylomicron level in neonate.
            >
            >
            > with warm regards
            > Sqn Ldr AK Garg
            > Gd splt paed,7 Air Force Hosp,Kanpur
            >
            >
            >
          • Madhuri Kanitkar
            Garg well managed. Since you have done a lit search can you sharre the long term followup required and outcome in such cases. Madhuri Kanitkar ... -- Col
            Message 5 of 8 , Mar 18, 2012
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              Garg well managed. Since you have done a lit search can you sharre the long term followup required and outcome in such cases.
              Madhuri Kanitkar

              On Fri, Mar 16, 2012 at 11:35 PM, rakhee.garg <rakhee.garg@...> wrote:
               

              Respected Seniors and Colleagues
              I would like to share my recent experience of managing a neonate.Comments are invited.

              case summary

              20 days old neonate a product of non-consanguineous marriage admitted to our hospital with h/o fever, high grade, intermittent, not feeding well, vomiting and lethargic. On examination HR 176/min, RR 64/min, temp 100 F, SPO2 98%, CFT <3sec, wt 3.8kg (B. WT 3.2Kg) pallor +ve, abdomen was distended, liver palpable 3cm below rt costal margin, spleen tip palpable On investigation Hb 8.6gm%, TLC 4000, Neutrophil 33%, lymphocyte 62%, platelet 1lac, CRP 60 and PBS S/O sepsis, CXR and Transcranial USG were WNL. Baby was started on broad spectrum antibiotic. After 48hrs of antibiotic, child responded partially but still fever persisting . Card test for MP and PBS for MP was sent and found to be positive for plasmodium Vivax. Baby was started on chloroquine, baby responded to treatment. Incidentally while dispatching the blood sample in plain sterile vacutainer, sample was found to be chylous . Our laboratory reported sample chylous in appearance, total cholesterol 220 mg/dl, Tgs 2039mg/dl, direct HDL 15mg/dl and LDL 107mg/dl. Test repeated by spectrometry and electrophoresis cholesterol 202 mg/dl, Triglycerides 1588 mg/dl, HDL 30.46 mg/dl, LDL 97.75 mg/dl, VLDL 73.79 mg/dL, Chylomicron nil , thyroid profile , BSL , S. Amylase,S. albumin were wnl. USG abdomen was s/o of hepatosplenomegaly with no feature s/o pancreatitis. There were no eruptive xanthomas, fundus examination was normal. Baby was born to 24 yrs old booked and immunized primigravida at term with birth wt 3.2kg. Perinatal period was uneventful. No family history of dyslipidaemia. Lipid profiles of mother shows mild increase in triglyceride level otherwise lipid profile of both parents were essentially normal. Child was diagnosed as a case of familial hypertriglyceridaemia (FHTG). Baby was managed with low fat milk, vit ADEK ,carnitine supplement and MCT oil. On follow up baby is thriving well and lipid profile achieved near normal over 1month on low fat milk, mct oil and fat soluble vit.Presently father is posted out to pathankot,hope parent has reported to maj Rahul for follow up.

              Neonatal hypertriglyceridaemia is extremely rare characterized by moderately elevated plasma triglyceride accompanied by modest elevations in cholesterol. VLDL is the major class of lipoproteins elevated in this disorder, which is referred to as type four hyperlipoproteinemia. The diagnosis of FHTG is suggested in our case by elevated plasma triglycerides 1588 mg/dl (30-86), VLDL 73.79 mg/dl (20-40), mildly elevated cholesterol 202 mg/dl (45-182) with normal HDL 30.46 mg/dl (30-70), LDL 97.75 mg/dl and Chylomicron. Secondary causes ruled out by normal blood sugar level, thyroid profile, LFT, RFT and no history of any drug intake except chloroquine, ceftriazone and amikacin. But there was similar case reported by MS Tullu etal in eight-month-old boy admitted for malaria and anemia, incidentally diagnosed as a case of FHTG due to lipemic serum .He had elevated serum triglycerides with normal serum cholesterol, but had no symptoms related to the primary disorder (FHTG). There is no case report/literature suggesting association of malaria with hypertriglyceridaemia. There are few case report of type 1 and type V hypertriglyceridaemia in neonatal period . But no case report or literature found suggesting type IV FHTG with such high level of triglyceride with normal chylomicron level in neonate.

              with warm regards
              Sqn Ldr AK Garg
              Gd splt paed,7 Air Force Hosp,Kanpur




              --
              Col Madhuri Kanitkar
              Senior Advisor Pediatrics
              Military Hospital Namkum
              Ranchi - Jharkhand

            • shamsher dalal
              Dear Garg This baby had malaria and blood counts were suggestive of decreased counts of all three cell lines. Malaria can cause macrophage activation syndrome
              Message 6 of 8 , Mar 19, 2012
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                Dear Garg
                This baby had malaria and blood counts were suggestive of decreased counts of all three cell lines. Malaria can cause macrophage activation syndrome like picture in which hypertriglyceridemia to the level seen in your case is sometimes seen. Bone marrow examination would have been of some help. As far as FHTG is concerned we should be careful of diagnosing it in the absence of positive family history (Autosomal dominant inheritence) and presenting during neonatal period. Normalization of triglyceride levels may be due to treatment of precipitating infection. Now trial of full strength milk and following of triglyceride levels may give hint to the diagnosis.
                Keep us updated.
                Best wishes
                --
                Wg Cdr  S S Dalal
                MD (Paed) DM (Neonatology)
                Classified Specialist (Paed) & Neonatologist
                Command Hospital (Air Force)
                Old Airport Road
                Bangalore- 560007
                India
                Moblie: +919900312725
              • Madhuri Kanitkar
                Dalal thanks for these inputs. The case in interesting and we request Garg to keep us posted M ... -- Col Madhuri Kanitkar Senior Advisor Pediatrics Military
                Message 7 of 8 , Mar 19, 2012
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                  Dalal thanks for these inputs. The case in interesting and we request Garg to keep us posted
                  M

                  On Mon, Mar 19, 2012 at 9:48 PM, shamsher dalal <dalalshamsher@...> wrote:
                   

                  Dear Garg

                  This baby had malaria and blood counts were suggestive of decreased counts of all three cell lines. Malaria can cause macrophage activation syndrome like picture in which hypertriglyceridemia to the level seen in your case is sometimes seen. Bone marrow examination would have been of some help. As far as FHTG is concerned we should be careful of diagnosing it in the absence of positive family history (Autosomal dominant inheritence) and presenting during neonatal period. Normalization of triglyceride levels may be due to treatment of precipitating infection. Now trial of full strength milk and following of triglyceride levels may give hint to the diagnosis.
                  Keep us updated.
                  Best wishes
                  --
                  Wg Cdr  S S Dalal
                  MD (Paed) DM (Neonatology)
                  Classified Specialist (Paed) & Neonatologist
                  Command Hospital (Air Force)
                  Old Airport Road
                  Bangalore- 560007
                  India
                  Moblie: +919900312725




                  --
                  Col Madhuri Kanitkar
                  Senior Advisor Pediatrics
                  Military Hospital Namkum
                  Ranchi - Jharkhand

                • sheila mathai
                  Great work Garg, but just for interest sake and food for thought I am sending this article... Surg Capt Sheila Mathai, VSMMD, DNB, DM (Neonatology)Senior
                  Message 8 of 8 , Mar 29, 2012
                  Great work Garg, but just for interest sake and food for thought I am sending this article...

                  Surg Capt Sheila Mathai, VSM
                  MD, DNB, DM (Neonatology)
                  Senior Adviser (Pediatrics & Neonatology)
                  Professor & Head of Department
                  Department of Pediatrics
                  INHS Asvini
                  Colaba
                  Mumbai 400005


                  --- On Sun, 3/18/12, Madhuri Kanitkar <mkanitkar15@...> wrote:

                  From: Madhuri Kanitkar <mkanitkar15@...>
                  Subject: Re: [defencepeds] case discussion
                  To: defencepeds@yahoogroups.com
                  Date: Sunday, March 18, 2012, 12:13 AM

                   

                  Garg well managed. Since you have done a lit search can you sharre the long term followup required and outcome in such cases.
                  Madhuri Kanitkar

                  On Fri, Mar 16, 2012 at 11:35 PM, rakhee.garg <rakhee.garg@...> wrote:
                   

                  Respected Seniors and Colleagues
                  I would like to share my recent experience of managing a neonate.Comments are invited.

                  case summary

                  20 days old neonate a product of non-consanguineous marriage admitted to our hospital with h/o fever, high grade, intermittent, not feeding well, vomiting and lethargic. On examination HR 176/min, RR 64/min, temp 100 F, SPO2 98%, CFT <3sec, wt 3.8kg (B. WT 3.2Kg) pallor +ve, abdomen was distended, liver palpable 3cm below rt costal margin, spleen tip palpable On investigation Hb 8.6gm%, TLC 4000, Neutrophil 33%, lymphocyte 62%, platelet 1lac, CRP 60 and PBS S/O sepsis, CXR and Transcranial USG were WNL. Baby was started on broad spectrum antibiotic. After 48hrs of antibiotic, child responded partially but still fever persisting . Card test for MP and PBS for MP was sent and found to be positive for plasmodium Vivax. Baby was started on chloroquine, baby responded to treatment. Incidentally while dispatching the blood sample in plain sterile vacutainer, sample was found to be chylous . Our laboratory reported sample chylous in appearance, total cholesterol 220 mg/dl, Tgs 2039mg/dl, direct HDL 15mg/dl and LDL 107mg/dl. Test repeated by spectrometry and electrophoresis cholesterol 202 mg/dl, Triglycerides 1588 mg/dl, HDL 30.46 mg/dl, LDL 97.75 mg/dl, VLDL 73.79 mg/dL, Chylomicron nil , thyroid profile , BSL , S. Amylase,S. albumin were wnl. USG abdomen was s/o of hepatosplenomegaly with no feature s/o pancreatitis. There were no eruptive xanthomas, fundus examination was normal. Baby was born to 24 yrs old booked and immunized primigravida at term with birth wt 3.2kg. Perinatal period was uneventful. No family history of dyslipidaemia. Lipid profiles of mother shows mild increase in triglyceride level otherwise lipid profile of both parents were essentially normal. Child was diagnosed as a case of familial hypertriglyceridaemia (FHTG). Baby was managed with low fat milk, vit ADEK ,carnitine supplement and MCT oil. On follow up baby is thriving well and lipid profile achieved near normal over 1month on low fat milk, mct oil and fat soluble vit.Presently father is posted out to pathankot,hope parent has reported to maj Rahul for follow up.

                  Neonatal hypertriglyceridaemia is extremely rare characterized by moderately elevated plasma triglyceride accompanied by modest elevations in cholesterol. VLDL is the major class of lipoproteins elevated in this disorder, which is referred to as type four hyperlipoproteinemia. The diagnosis of FHTG is suggested in our case by elevated plasma triglycerides 1588 mg/dl (30-86), VLDL 73.79 mg/dl (20-40), mildly elevated cholesterol 202 mg/dl (45-182) with normal HDL 30.46 mg/dl (30-70), LDL 97.75 mg/dl and Chylomicron. Secondary causes ruled out by normal blood sugar level, thyroid profile, LFT, RFT and no history of any drug intake except chloroquine, ceftriazone and amikacin. But there was similar case reported by MS Tullu etal in eight-month-old boy admitted for malaria and anemia, incidentally diagnosed as a case of FHTG due to lipemic serum .He had elevated serum triglycerides with normal serum cholesterol, but had no symptoms related to the primary disorder (FHTG). There is no case report/literature suggesting association of malaria with hypertriglyceridaemia. There are few case report of type 1 and type V hypertriglyceridaemia in neonatal period . But no case report or literature found suggesting type IV FHTG with such high level of triglyceride with normal chylomicron level in neonate.

                  with warm regards
                  Sqn Ldr AK Garg
                  Gd splt paed,7 Air Force Hosp,Kanpur




                  --
                  Col Madhuri Kanitkar
                  Senior Advisor Pediatrics
                  Military Hospital Namkum
                  Ranchi - Jharkhand

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