This lecture was conducted during the Nephrology Unit Grand Ground by Registrar under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida, Chairman of Department of Medicine. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

HYPERTRIGLYCERIDEMIA HYPERTRIGLYCERIDEMIA AND PLASMAPHERESISAND PLASMAPHERESIS

Presented by:Dr. Habib Ur Rahman

RegistrarJune 2008

RECENT TRIALSRECENT TRIALS

Mechanism of TG.SynthesisMechanism of TG.Synthesis

Causes►Hypertriglyceridemia has many causes,

including familial and genetic syndromes, metabolic disease, and drugs.

►Genetic causes: ►Abnormalities of the enzyme pathway

for chylomicron metabolism are the best-characterized genetic causes of hTG. However, less clearly defined inheritable disorders are more frequent causes of elevated TGs.

Table 2. Fredrickson Dyslipidemia Classification

Type Elevated Lipoprotein

Total Cholesterol Level

Triglyceride Level

Relative Frequency

I CM* Normal ++ <1%

IIa LDL ++ Normal 10%

(FHC)        

IIb LDL/VLDL ++ + 40%

(FCH)        

III IDL + + <1%

IV VLDL Normal to+ ++ 45%

(FHT)        

V CM + ++ 5%

  VLDL      

* CM, chylomicron; LDL, low-density lipoprotein; VLDL, very low-density lipoprotein; IDL, intermediate density lipoprotein; FHC, familial hypercholesterolemia; FCH, familial combined hyperlipidemia; FHT, familial hypertriglyceridemia.

Metabolic causesMetabolic causes

Diabetes: Diabetes: Uncontrolled diabetes mellitus, Uncontrolled diabetes mellitus,

►Patients with type 1 diabetes mellitusPatients with type 1 diabetes mellitus►with uncontrolled type 2 diabetes mellitus and with uncontrolled type 2 diabetes mellitus and

hyperinsulinemia hyperinsulinemia

Obesity: Obesity: Hypothyroidism: Hypothyroidism: Nephrotic syndrome:Nephrotic syndrome:

Other causes of hTGOther causes of hTG► Alcohol:Alcohol:

Excessive alcohol intake is frequent cause of hTG. Excessive alcohol intake is frequent cause of hTG. ► High-carbohydrate dietsHigh-carbohydrate diets (>60% of caloric (>60% of caloric

intake) intake) ► Acute pancreatitisAcute pancreatitis

may cause substantial elevations in TGs by may cause substantial elevations in TGs by unknown mechanisms. However, much more unknown mechanisms. However, much more frequently, severe hTG causes acute pancreatitis. frequently, severe hTG causes acute pancreatitis. In patients presenting with acute pancreatitis and In patients presenting with acute pancreatitis and TGs greater than 1000 mg/dL, not assuming that TGs greater than 1000 mg/dL, not assuming that the TGs are the cause of the pancreatitis is the TGs are the cause of the pancreatitis is prudent. Other causes, such as common bile duct prudent. Other causes, such as common bile duct obstruction and alcoholism, must be considered obstruction and alcoholism, must be considered as possible etiologies as possible etiologies

► PregnancyPregnancy

Table 3. Medications That Elevate Triglyceride

Atypical anti-psychotics

Beta blockers

Bile acid binding resins

Estrogen (in higher dose oral contraceptives and unopposed oral estrogen)

Glucocorticoids

Immunosuppressants

Isotretinoin

Protease inhibitors

Tamoxifen

Thiazides

HypertriglyceridemiaHypertriglyceridemia

Copyright ©2002 Canadian Medical Association or its licensors

Fung, M. A. et al. CMAJ 2002;167:1261-1266

Copyright ©2002 Canadian Medical Association or its licensors

Fung, M. A. et al. CMAJ 2002;167:1261-1266

Obesity Obesity

 Classification of Triglyceride Levels

Classification Triglyceride Level (mg/dL)

Normal <150 (1.7 m mol/L)

Borderline high 150 to 199 (1.7-2.26 m mol/L)

High 200 to 499 (2.26-5.65 m mol/L)

Very high >500 (5.65 m mol/L)

Table 6. Basic Laboratory Evaluation for Confirmed Hypertriglyceridemia

Serum urea nitrogen

Creatinine

Fasting glucose and lipid profile.

Fasting insulin level (if metabolic syndrome is suspected)

Liver function

Serum electrolyte

Urinalysis

SERUM AMYLASE

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001;285:2486-2497.

Treatment Categories, LDL-C Treatment Categories, LDL-C Goals and Cut pointsGoals and Cut points

Risk CategoryRisk Category LDL-C GoalLDL-C Goal

Consider Consider Drug Drug

TherapyTherapy

CHD or CHD or CHD risk CHD risk equivalentequivalent <100 mg/dL<100 mg/dL 130 130

mg/dL*mg/dL*2 Risk Factors2 Risk Factors

10-yr risk 10–10-yr risk 10–20%20%

10-yr risk <10%10-yr risk <10%

<130 mg/dL<130 mg/dL

<130 mg/dL<130 mg/dL130 mg/dL130 mg/dL

160 mg/dL160 mg/dL

<2 Risk Factors<2 Risk Factors <160 mg/dL<160 mg/dL 190 mg/dL190 mg/dL

* 100–129 mg/dL = after TLC, consider statin, niacin, or fibrate therapy

Table 3. Initial Management of Hypertriglyceridemia

Intervention Description Comments

Counsel patients about therapeutic lifestyle changes

Body weight control, regular physical activity, tobacco-use cessation, avoidance of high-carbohydrate foods, diet low in saturated fat and sugar

Patients with triglyceride levels above 1,000 mg per dL (11.30 mmol per L) should immediately start a very low-fat diet

Screen for metabolic syndrome Constellation of increased abdominal circumference and low HDL-C levels, high triglyceride and blood sugar levels, and elevated blood pressure

Diagnosis and management remain controversial

Search for secondary causes Nephrotic syndrome, diabetes, chronic renal failure, hypothyroidism, various medications

Optimizing glycemic control may improve hypertriglyceridemia

Search for acquired causes Overweight and obesity, excessive alcohol intake, high carbohydrate intake, tobacco use

-

Determine cardiac risk profile Determine cardiac risk factors, and stratify the patient's 10-year risk of coronary heart disease using Framingham risk calculators

-

Physicians should stratify the patient's risk to determine a lipid treatment goal. High-risk patients

Copyright ©2002 Canadian Medical Association or its licensors

Fung, M. A. et al. CMAJ 2002;167:1261-1266

Management of Hypertriglyceridemia

Copyright ©2002 Canadian Medical Association or its licensors

Fung, M. A. et al. CMAJ 2002;167:1261-1266

Fig. 2: Mechanism of niacin action

PLASMAPHERESISPLASMAPHERESIS

PLASMAPHARESISPLASMAPHARESIS

Plasmapheresis: Basic Plasmapheresis: Basic PrinciplesPrinciples

Membrane vs. CentrifugationMembrane vs. Centrifugation

► In the US, most TPE is performed by In the US, most TPE is performed by centrifugation. centrifugation. One machine can One machine can do all apheresis procedures. do all apheresis procedures.

►Double filtration method: first Double filtration method: first membrane separates plasma from membrane separates plasma from cellular portion and second cellular portion and second membrane separates globulin from membrane separates globulin from albumin.albumin.

►LDL apheresis: using membrane LDL apheresis: using membrane coated with antibody to LDL, only coated with antibody to LDL, only LDL cholesterol can be removed. LDL cholesterol can be removed.

Continuous vs. IntermittentContinuous vs. Intermittent

►Continuous: Continuous: COBE SpectraCOBE Spectra, Fenwall CS3000, Fenwall CS3000

► Intermittent: Haemonetics Intermittent: Haemonetics

PlasmaPlatelets

Lymphocytes

Monocytes

GranulocytesNeocytes

Erythrocytes

Blood Components Separated by Centrifugation

Plasma Exchange

TPE: Available techniques... • Cascade or secondary filtration: Separated

blood is perfused through a plasma filter (1) to remove certain plasma elements. The second column (2) (cascade) absorbs the element and the plasma is returned to the patient.

1 2 PATIENT

TPE: Available techniques

Qb 100-150

Hct 25-45%

TMP <50 mmHg

=Plasma effluent

Plasma removal is affected by:• Qb• Hct• Pore Size• TMP

Pore Size

Rationale of Plasma Rationale of Plasma ExchangeExchange

►The existence of a known The existence of a known pathogenic substance in the plasma.pathogenic substance in the plasma. IgG, IgM, phytanic acid, cytokines IgG, IgM, phytanic acid, cytokines

(?)(?)►The possibility of removing this The possibility of removing this

substance more rapidly than it can substance more rapidly than it can be renewed in the body.be renewed in the body.

Efficiency of removal is greatest early in the procedure and diminishes progressively during the exchange.

Small vs. Large Volume Small vs. Large Volume ExchangeExchange

►1.0 plasma volume exchange: 1.0 plasma volume exchange: minimizes time required for each minimizes time required for each procedure but may need more procedure but may need more frequent procedures.frequent procedures.

►2.0 – 3.0 plasma volume exchange: 2.0 – 3.0 plasma volume exchange: greater initial diminution of pathologic greater initial diminution of pathologic substance but requiring considerably substance but requiring considerably more time to perform the procedure.more time to perform the procedure.

Mechanical Removal of Mechanical Removal of AntibodiesAntibodies

►When antibody is rapidly and When antibody is rapidly and massively decreased by TPE, antibody massively decreased by TPE, antibody synthesis increases rapidly. synthesis increases rapidly.

►This rebound response complicates This rebound response complicates treatment of autoimmune diseases.treatment of autoimmune diseases.

► It is usually combined with immune It is usually combined with immune suppressive therapy.suppressive therapy.

Replacement FluidReplacement Fluid

►Fresh frozen plasma – TTP, liver Fresh frozen plasma – TTP, liver failure, coagulopathy with inhibitors, failure, coagulopathy with inhibitors, patients with coagulopathy, immediate patients with coagulopathy, immediate post surgery.post surgery.

►Cryopoor plasma – TTPCryopoor plasma – TTP►5% albumin – Most cases.5% albumin – Most cases.

PlasmapheresisPlasmapheresis

► and plasma exchange may be considered medically and plasma exchange may be considered medically necessary for any of the conditions listed below:necessary for any of the conditions listed below:

► Myasthenia gravis in crisis or as part of Myasthenia gravis in crisis or as part of preoperative preparation preoperative preparation

► Hyperviscosity syndromes associated with multiple Hyperviscosity syndromes associated with multiple myeloma, Waldenström's macroglobulinemia, or myeloma, Waldenström's macroglobulinemia, or other conditions other conditions

► Thrombotic thrombocytopenic purpura (TTP) Thrombotic thrombocytopenic purpura (TTP) ► Hemolytic uremic syndrome (HUS) Hemolytic uremic syndrome (HUS) ► Idiopathic thrombocytopenic purpura in emergency Idiopathic thrombocytopenic purpura in emergency

situations situations ► Guillain-Barré syndrome in severely ill patients who Guillain-Barré syndrome in severely ill patients who

are diagnosed with grades 3-5 disease (see grading are diagnosed with grades 3-5 disease (see grading below) below)

PlasmapheresisPlasmapheresis► Chronic inflammatory demyelinating polyneuropathy Chronic inflammatory demyelinating polyneuropathy

meeting all of the following three criteria: meeting all of the following three criteria: Associated with life-threatening symptoms or severe Associated with life-threatening symptoms or severe

disability; disability; Diagnosed by slowing of nerve conduction velocity on Diagnosed by slowing of nerve conduction velocity on

EMG/NCS and elevated spinal fluid protein on lumbar EMG/NCS and elevated spinal fluid protein on lumbar puncture; and puncture; and

Failed to respond to previous treatment with prednisone and Failed to respond to previous treatment with prednisone and intravenous immunoglobulins (IVIg) intravenous immunoglobulins (IVIg)

► IgA or IgG paraproteinemia polyneuropathy IgA or IgG paraproteinemia polyneuropathy ► HELLP syndrome of pregnancy HELLP syndrome of pregnancy ► Post-transfusion purpura Post-transfusion purpura ► Progressive renal failure due to anti-basement Progressive renal failure due to anti-basement

membrane antibodies (i.e., Goodpasture's syndrome membrane antibodies (i.e., Goodpasture's syndrome ► Acute fulminant CNS demyelination associated with Acute fulminant CNS demyelination associated with

multiple sclerosis or other idiopathic inflammatory multiple sclerosis or other idiopathic inflammatory demyelinating diseases, such as transverse myelitis, demyelinating diseases, such as transverse myelitis, which may proceed to severe cognitive dysfunction, which may proceed to severe cognitive dysfunction, hemiplegia, paraplegia or quadriplegia hemiplegia, paraplegia or quadriplegia

PlasmapheresisPlasmapheresis

► Cryoglobulinemia Cryoglobulinemia ► Chronic myelogenous leukemia Chronic myelogenous leukemia ► Chronic demyelinating gammopathy Chronic demyelinating gammopathy ► Leukapheresis in the treatment of leukemia Leukapheresis in the treatment of leukemia ► Life-threatening rheumatoid vasculitis Life-threatening rheumatoid vasculitis ► Pure red cell aplasia unresponsive to steroid and Pure red cell aplasia unresponsive to steroid and

immunosuppressive therapy immunosuppressive therapy ► Plasma perfusion of charcoal filter for treatment of Plasma perfusion of charcoal filter for treatment of

pruritus of cholestatic liver disease pruritus of cholestatic liver disease ► Prior to solid organ transplant, treatment of Prior to solid organ transplant, treatment of

patients at high risk of antibody-mediated rejection, patients at high risk of antibody-mediated rejection, including highly sensitized patients, and those including highly sensitized patients, and those receiving an ABO incompatible organ receiving an ABO incompatible organ

► Following solid-organ transplant, for the treatment Following solid-organ transplant, for the treatment of antibody-mediated rejection of antibody-mediated rejection

PlasmapharesisPlasmapharesis►is considered investigational for is considered investigational for

all other applications, including all other applications, including but not limited to:but not limited to: Rheumatoid arthritis Rheumatoid arthritis Scleroderma (systemic sclerosis) Scleroderma (systemic sclerosis) Systemic lupus erythematosus Systemic lupus erythematosus Polymyositis and dermatomyositis Polymyositis and dermatomyositis Inclusion body myositis Inclusion body myositis Pemphigus Pemphigus Guillain-Barré syndrome, grades 1-2 Guillain-Barré syndrome, grades 1-2 Multiple sclerosis in the absence of Multiple sclerosis in the absence of

acute fulminant onset acute fulminant onset

PlasmapharesisPlasmapharesis Amyotrophic lateral sclerosis Amyotrophic lateral sclerosis Paraneoplastic syndromes including Paraneoplastic syndromes including

Lambert-Eaton myasthenic syndrome Lambert-Eaton myasthenic syndrome Paraproteinemic polyneuropathy, including Paraproteinemic polyneuropathy, including

monoclonal gammopathy of undetermined monoclonal gammopathy of undetermined significance (MGUS) significance (MGUS)

Chronic fatigue syndrome Chronic fatigue syndrome Regional enteritis (Crohn's disease) Regional enteritis (Crohn's disease) Rapidly progressive glomerulonephritides, Rapidly progressive glomerulonephritides,

excluding those related to anti-basement excluding those related to anti-basement membrane immunoglobulins (i.e., membrane immunoglobulins (i.e., Goodpasture’s syndrome -- covered above) Goodpasture’s syndrome -- covered above)

Asthma Asthma Stiff man syndrome Stiff man syndrome Acute pancreatitis related to Acute pancreatitis related to

hyperlipidemiahyperlipidemia

PLASMAPHARESIS IN 10 CASESPLASMAPHARESIS IN 10 CASESKyriakidisKyriakidis AV AV, , RaitsiouRaitsiou B B, , Sakagianni ASakagianni A, , Harisopoulou VHarisopoulou V, , Pyrgioti MPyrgioti M, , Panagopoulou APanagopoulou A, ,

Vasilakis NVasilakis N, , Lambropoulos SLambropoulos S..Intensive Care Unit, General Hospital Sismanogleion, Athens, Greece. alkidi@hotmail.comIntensive Care Unit, General Hospital Sismanogleion, Athens, Greece. alkidi@hotmail.com

PLASMAPHARESIS IN 10 CASESPLASMAPHARESIS IN 10 CASES► KyriakidisKyriakidis AV AV, , RaitsiouRaitsiou B B, , SakagianniSakagianni A A, , HarisopoulouHarisopoulou V V, , PyrgiotiPyrgioti M M, ,

PanagopoulouPanagopoulou A A, , VasilakisVasilakis N N, , LambropoulosLambropoulos S S.. Intensive Care Unit, General Hospital Sismanogleion, Athens, Greece. Intensive Care Unit, General Hospital Sismanogleion, Athens, Greece.

alkidi@hotmail.comalkidi@hotmail.com► severe hyperlipidemic pancreatitis when triglyceride severe hyperlipidemic pancreatitis when triglyceride

levels exceed 11.3 mmol/l.levels exceed 11.3 mmol/l.► 10 patients were evaluated the therapeutic guidelines 10 patients were evaluated the therapeutic guidelines

for severe hyperlipidemic pancreatitis.for severe hyperlipidemic pancreatitis.► ► RESULTS:RESULTS:► Standard treatment was essential for all the patients Standard treatment was essential for all the patients ► but plasmapheresis was the procedure that lowered the but plasmapheresis was the procedure that lowered the

triglyceride and lipid levels in all cases. triglyceride and lipid levels in all cases. ► It improved abdominal pain, clinical state, and signs It improved abdominal pain, clinical state, and signs

and symptoms of the disease. and symptoms of the disease. ► Two patients underwent surgery due to infection of the Two patients underwent surgery due to infection of the

necrotic segments and one of them died. necrotic segments and one of them died. ► Follow-up lasted 4-54 months with no recurrences of Follow-up lasted 4-54 months with no recurrences of

pancreatitis.pancreatitis.

Management of acute severe Management of acute severe hyperlipidemic pancreatitis.hyperlipidemic pancreatitis.

► CONCLUSION: CONCLUSION: Hyperlipidemic pancreatitis should initially Hyperlipidemic pancreatitis should initially

be treated conservatively study shows that be treated conservatively study shows that standard treatment is essential, standard treatment is essential,

. Plasmapheresis is a method that has . Plasmapheresis is a method that has lately been used successfully for lately been used successfully for hyperlipidemic pancreatitis. It seems hyperlipidemic pancreatitis. It seems that all therapeutic measures should that all therapeutic measures should be applied as early as possible, within be applied as early as possible, within the first 48 h.the first 48 h.

► PMID: 16940728 [PubMed - indexed for MEDLINE]PMID: 16940728 [PubMed - indexed for MEDLINE]

Plasmapheresis in the management of acute severe Plasmapheresis in the management of acute severe hyperlipidemic pancreatitis: report of 5 cases. hyperlipidemic pancreatitis: report of 5 cases. 2006 S. Karger 2006 S. Karger

AG, BaselAG, Basel

►Plasma exchange lowered the Plasma exchange lowered the lipid level and TGLs in all 5 cases. lipid level and TGLs in all 5 cases. It also improved abdominal pain,It also improved abdominal pain, Complications of treatment were not Complications of treatment were not

encountered, encountered, none of the patients died and none of the patients died and only 1 patient underwent surgery.only 1 patient underwent surgery. Follow-up of the patients lasted 4-28 Follow-up of the patients lasted 4-28

months, and recurrence of pancreatitis was months, and recurrence of pancreatitis was not noted. not noted.

..

► One patient was treated with one One patient was treated with one plasmapheresis that allowed a dramatic plasmapheresis that allowed a dramatic (89%) decrease in the triglycerides level. (89%) decrease in the triglycerides level.

► The acute pancreatitis resolved and the The acute pancreatitis resolved and the patient was discharged from the intensive patient was discharged from the intensive care unit at day 5 with lipids and pancreatic care unit at day 5 with lipids and pancreatic enzyme levels within normal range. enzyme levels within normal range.

PMID: 14569604 [PubMed - indexed for PMID: 14569604 [PubMed - indexed for MEDLINE]MEDLINE]

First case of acute pancreatitis induced by First case of acute pancreatitis induced by hypertriglyceridemia in the settinghypertriglyceridemia in the settingof an uncontrolled cytophagic histiocytic panniculitis of an uncontrolled cytophagic histiocytic panniculitis successfully treated by plasmapheresissuccessfully treated by plasmapheresis

Plasmapheresis as an adjuvant therapy for Plasmapheresis as an adjuvant therapy for hypertriglyceridemia-induced pancreatitis.hypertriglyceridemia-induced pancreatitis.

► IskandarIskandar SB SB, , Olive KEOlive KE.. Department of Internal Medicine, James H. Quillen College of Department of Internal Medicine, James H. Quillen College of

Medicine, East Tennessee State University, Johnson City, TN Medicine, East Tennessee State University, Johnson City, TN 37614, USA.37614, USA.

► Hypertriglyceridemia is an uncommon cause of Hypertriglyceridemia is an uncommon cause of pancreatitis. pancreatitis.

► A serum triglyceride level of more then 1000 to A serum triglyceride level of more then 1000 to 2000 mg/dL(13.1 to 26.2 m mole/L) is an 2000 mg/dL(13.1 to 26.2 m mole/L) is an identifiable risk factor. identifiable risk factor.

► Interestingly, serum pancreatic enzyme levels Interestingly, serum pancreatic enzyme levels may be normal or only minimally elevated in may be normal or only minimally elevated in such cases. such cases.

► The reduction of triglyceride level to below 1000 The reduction of triglyceride level to below 1000 mg/dL (13.1 m mole/L) effectively prevents mg/dL (13.1 m mole/L) effectively prevents further episodes of pancreatitis. further episodes of pancreatitis.

Plasmapheresis as an adjuvant therapy for Plasmapheresis as an adjuvant therapy for hypertriglyceridemia-induced pancreatitis.hypertriglyceridemia-induced pancreatitis.

Iskandar SBIskandar SB, , Olive KEOlive KE..Department of Internal Medicine, James H. Quillen College of Medicine, East Department of Internal Medicine, James H. Quillen College of Medicine, East

Tennessee State University, Johnson City, TN 37614, USA.Tennessee State University, Johnson City, TN 37614, USA.

► The mainstay of treatment for the The mainstay of treatment for the hypertriglyceridemia associated with hypertriglyceridemia associated with pancreatitis includes pancreatitis includes dietary restriction of fat and administration of dietary restriction of fat and administration of

lipid-lowering agents. lipid-lowering agents. ► It is thought that within 24 to 48 hours of It is thought that within 24 to 48 hours of

the onset of pancreatitis, in the majority of the onset of pancreatitis, in the majority of patients, triglyceride levels fall rapidly as a patients, triglyceride levels fall rapidly as a result of fasting status, as the absorption of result of fasting status, as the absorption of chylomicrons to the blood is cut off. chylomicrons to the blood is cut off.

► Experiences with plasmapheresis are Experiences with plasmapheresis are limited. limited.

Hypertriglyceridemia: apheretic treatment. Hypertriglyceridemia: apheretic treatment. treated 15 treated 15 cases of hypertriglyceridemia complicating the course of cases of hypertriglyceridemia complicating the course of

patients receiving Cyclosporin A after bone marrow patients receiving Cyclosporin A after bone marrow transplantationtransplantation

► GianniniGiannini G G, , ValbonesiValbonesi M M, , MorelliMorelli F F, , CarlierCarlier P P, , De Luigi MCDe Luigi MC, , DejanaDejana AM AM, , RuzzenentiRuzzenenti MR MR..

► Patients with extremely high triglyceride levels Patients with extremely high triglyceride levels and associated lipemia are at high risk for acute and associated lipemia are at high risk for acute pancreatitis. pancreatitis. Two factors can increase triglyceride-rich Two factors can increase triglyceride-rich

lipoproteins;lipoproteins;► one is overproduction and other is a defect in clearance.one is overproduction and other is a defect in clearance.► Either mechanism can cause hypertriglyceridemia and both Either mechanism can cause hypertriglyceridemia and both

may exist simultaneously.may exist simultaneously.► Causes can be either primary or secondary. Causes can be either primary or secondary.

► Plasmapheresis is efficacious for severe Plasmapheresis is efficacious for severe Hypertriglyceridemia in patients who have not Hypertriglyceridemia in patients who have not responded to previous therapies.. responded to previous therapies.. PMID: 16288440 [PubMed - indexed for PMID: 16288440 [PubMed - indexed for MEDLINE]MEDLINE]

RANSON CRITERIARANSON CRITERIA

► Initial 24 hrsInitial 24 hrs

1.Age >55 years1.Age >55 years

2.Glucose >than 2.Glucose >than 200 mgm/dl200 mgm/dl

3.WBC > 16,000 3.WBC > 16,000 cells/mic Lcells/mic L

4.LDH >350 4.LDH >350 IU/literIU/liter

5.AST >250IU/liter5.AST >250IU/liter

► Subsequent 48 hrsSubsequent 48 hrs1.Art o1.Art o22tension tension <60mmHg<60mmHg

2.Bun Increase 2.Bun Increase >8mg/dl>8mg/dl

3.Ca < 8mg/dl3.Ca < 8mg/dl

4.Base deficit 4.Base deficit >4meq/liter>4meq/liter

5.Estimated fluid 5.Estimated fluid sequestration >6literssequestration >6liters

6.Fall n Hct >10%6.Fall n Hct >10%

Mortality prediction (as per Mortality prediction (as per Ranson criteria) Ranson criteria)

AA. . < 3 signs = 1%< 3 signs = 1%

BB. Three to Four signs=11%. Three to Four signs=11%

CC. Five to six signs=33%. Five to six signs=33%

D. D. >Six signs= 100%>Six signs= 100%

IMRIE,S CRITERIAIMRIE,S CRITERIA

► During first 24 During first 24 hourshours

1.Age>55 yrs1.Age>55 yrs

2.WBC >15x 102.WBC >15x 10 9 9/l/l

3.Blood glucose 3.Blood glucose >10mmol/l>10mmol/l

4.Plasma 4.Plasma Urea>16mmol/lUrea>16mmol/l

5.Pao5.Pao22<8Kpa<8Kpa

6.Pl ca<2.0mmo/l6.Pl ca<2.0mmo/l

7.Pl albumin<32g/l7.Pl albumin<32g/l

8.LDH>600 8.LDH>600 u/l(n=250)u/l(n=250)

9.AST or ALT >100 9.AST or ALT >100 u/lu/l

GLASGOW CRITERIAGLASGOW CRITERIA

►Any time during Any time during First 48hrs after First 48hrs after admission;admission;WBC >15000 Cu/mmWBC >15000 Cu/mmBlood Blood

glucose>10mmol/lglucose>10mmol/lBUN >16mmol/LBUN >16mmol/LArt poArt po22,< 60mmHg,< 60mmHg

Ser ca. <2.0 ml/lSer ca. <2.0 ml/lSer Albumin<32gm/lSer Albumin<32gm/lSer LDH Ser LDH

>600u/L(n=250)>600u/L(n=250)AST Or ALT >200u/lAST Or ALT >200u/l

APACHEII-variablesAPACHEII-variables

1.1. TempTemp

2.2. Mean Art PressureMean Art Pressure

3.3. Heart RateHeart Rate

4.4. Resp rateResp rate5.5. Oxygenation(PaoOxygenation(Pao2)2)

6.6. Arterial PhArterial Ph

1.1. Serum sodiumSerum sodium

2.2. SerumPottasiumSerumPottasium

3.3. Serum creatinineSerum creatinine

4.4. HaematocritHaematocrit

5.5. WCCWCC

6.6. Glasgow coma Glasgow coma scalescale

Apache II score(Sum of Apache II score(Sum of A+B+C)A+B+C)

► A=+4 to 0 pointsA=+4 to 0 points TEMP>41=4,<29=4TEMP>41=4,<29=4 Mean Art Pr>160=4Mean Art Pr>160=4

<49=4 <49=4 Heart & Resp rateHeart & Resp rate

OXYGENATIONOXYGENATIONART PHART PHSer Na,K,Creat,Ser Na,K,Creat,

HCT,WBCHCT,WBC GLASGOW COMA ScoreGLASGOW COMA Score

► BB=Age <44=0 pts=Age <44=0 pts >75=6points>75=6points

► CC=Chronic Health =Chronic Health pointspoints H/o organ insufficiency H/o organ insufficiency

Liver,CVS,Resp,Renal, ,ILiver,CVS,Resp,Renal, ,Immunocompromisedmmunocompromised

► APACHE SCORE42=90% APACHE SCORE42=90% MortMort

FUTURE DIRECTIVESFUTURE DIRECTIVES

1.This modality of treatment needs 1.This modality of treatment needs further explorationfurther exploration

2.Large prospective clinical trials are 2.Large prospective clinical trials are needed to confirm it,s beneficial role in needed to confirm it,s beneficial role in treatment of Hyperlipidemia.treatment of Hyperlipidemia.

3.In future it will be adjunctive therapy 3.In future it will be adjunctive therapy or may be the sole therapy to acute or may be the sole therapy to acute pancreatitis.pancreatitis.

ReferencesReferences

► Harrison,s principles of internal medicine.Harrison,s principles of internal medicine.► E. medicineE. medicine► DigestionDigestion► CMAJCMAJ► PUBMEDPUBMED► Journal of american family physiciansJournal of american family physicians► AMERICAN JOURNAL OF GASTROENTEROLOGYAMERICAN JOURNAL OF GASTROENTEROLOGY► Journal american college of physiciansJournal american college of physicians► Comperehensive clinical nephrologyComperehensive clinical nephrology► Massry and Glassok,s text book of nephrologyMassry and Glassok,s text book of nephrology► American association of family physicianAmerican association of family physician