GTT & ITS INTERPRETATION, GTT IN PREGNANCY, COMA & ITS D/D,KETOSIS,LACTIC ACIDOSIS & HYPEROSMOLAR COMA

DR. ANILJEET SINGH, PG 2nd YR, DEPTT. OF BIOCHEMISTRY, PGIMS, ROHTAK.

GLUCOSE TOLERANCE TEST

DIAGNOSIS OF DM DEPENDS SOLELY ON DEMONSTRATION OF HYPERGLYCEMIA

EASY FOR DM TYPE 1 DIFFICULT FOR DM TYPE 2
1. 2.

ORAL GTT IS MORE SENSITIVE THAN FBG EARLY IN COURSE OF TYPE 2 DM. ALL PERSONS HAVING FPG > 140 mg/dl HAVE 2 HR GLUCOSE > 200 mg/dl.

World wide epidemic

India: 2000:32 mill 2020: 81 mill

Zimmet, Nature 2001

GLUCOSE / CARBOHYDRATE TOLERANCE

THE ABILITY OF THE BODY TO UTILIZE CARBOHYDRATES MAY BE KNOWN BY MEASURING ITS CARBOHYDRATE TOLERANCE WHICH IS INDICATED BY BLOOD GLUCOSE CURVE FOLLOWING GLUCOSE LOAD UNDER STANDARD CONDITIONS.

INDICATIONS OF ORAL GTT

TO CONFIRM THE DIAGNOSIS OF DM. PTS. WITH TRANSIENT OR SUSTAINED GLYCOSURIA,HAVING NO S/S OF DM WITH NORMAL FBG & PPBG. PTS. WIYH S/S OF DM HAVING NO GLYCOSURIA & NORMAL FBG. GLYCOSURIA A/W THYROTOXICOSIS ,INFECTION ,SEPSIS, LIVER DISEASE & PREGNANCY. STRONG FAMILY H/O DM BUT NO OVERT SYMPTOMS. IN CASES OF IMPAIRED GLUCOSE TOLERANCE (IGT). TO DIAGNOSE GESTATIONAL DIABETES.

EVALUATION OF NON DIABETIC GLYCOSURIA. DIAGNOSIS OF INSULIN RESISTANCE PTS. WITH OR WITHOUT S/S OF DM HAVING ONE ABNORMAL VALUE. POPULATION STUDIES FOR EPIDEMIOLOGICAL DATA.

CONTRAINDICATIONS - CONFIRMED C/O DM. - ACUTELY ILL PATIENTS.

NO ROLE IN FOLLOW UP OF THE PATIENT.

PREPARATION OF THE PATIENT

COMPLETE MENTAL OR PHYSICAL REST. ENSURE OVERNIGHT FASTING. ABSTENANCE FROM SMOKING & STERNOUS EXERCISE ON THE PREVIOUS DAY. NORMAL UNRESTRICTED CARB DIET FOR THREE PREVIOUS DAYS, PRIOR TO GTT. DISCONTINUE ALL THE DRUGS AFFECTING THE CARBOHYDRATE METABOLISM.

PROCEDURE FOR GTT

AFTER OVERNIGHT FASTING, VENOUS BLOOD IS COLLECTED ( FASTING SAMPLE). SIMILARLY; BLADDER EMPTIED, URINE COLLECTED FOR GLU. & KETONE BODIES ESTIMATION ( FASTING SAMPLE). FOR ADULTS; GLUCOSE LOAD OF 75 g DISSOLVED IN 250-300 ml OF WATER IS GIVEN TO THE SUBJECT TO DRINK IN 5 min. FOR CHILDREN; GLUCOSE LOAD OF 1.75 g/Kg BODY WEIGHT IS GIVEN. FIVE VENOUS SAMPLES & URINE SAMPLES ARE COLLECTED AT HOURLY INTERVAL FOR 2 & HOURS.

NOW-A-DAYS, IN EUROPEON SETTINGS THIS TEST IS ALSO DONE BY GIVING 100 gm GLUCOSE & TAKING FIVE SIMILAR SAMPLES AT 1 HOURLY INTERVAL. ALL THE FIVE BLOOD & URINE SAMPLES ARE ESTIMATED FOR GLUCOSE & GLUCOSE + KETONE BODIES RESPECTIVELY. GLUCOSE TOLERANCE CURVE IS PLOTTED BETWEEN BLOOD GLUCOSE LEVEL & THE TIME OF SAMPLING.

GTT RESPONSE
NORMAL GTT
BLOOD GLUCOSE mg/dl URINE GLUCOSE

0 HOUR 1/2 HOUR 1 HOUR 1 1/2 HRS 2 HRS 2 1/2 HRS 75 NEG 130 NEG 230 PP 130 NEG 200 PP 300 PPP 130 P 220 PP 90 NEG 150 NEG 280 PP 345 PPP 139 P 190 P 115 NEG 100 NEG 260 PP 365 PPPP 110 P 110 NEG 95 NEG 65 NEG 220 PP 350 PPP 76 NEG 170 NEG / P 330 PPP

BLOOD SUGAR / URINE SUGAR VALUES

MODERATE DM SEVERE DM

BLOOD GLUCOSE mg/dl URINE GLUCOSE BLOOD GLUCOSE mg/dl URINE GLUCOSE

RENAL GLYCOSURIA LAG CURVE

BLOOD GLUCOSE mg/dl URINE GLUCOSE

BLOOD GLUCOSE mg/dl 90 URINE GLUCOSE NEG / P

90 85 NEG / P NEG / P 80 NEG 85 NEG 65 NEG 80 NEG

FLAT CURVE

80 NEG 75 NEG

BLOOD GLUCOSE mg/dl URINE GLUCOSE

GTC OF CAPILLARY BLOOD 1. RISE BEGINS EARLIER. 2. PEAK REACHED AT 30- 45 min. 3. LEVEL IN CAPILLARY BLOOD MAY BE 2070mg HIGHER THAN VENOUS BLOOD. 4. RETURN TO FASTING LEVEL MAY TAKE EVEN MORE THAN 3 1/2- 4 HOURS OR EVEN MORE.

DECREASED GLUCOSE TOLERANCE

1. 2. 3.

DM HYPERACTIVITY OF ANT PIT & A.CORTEX HORMONES HYPERTHYROIDISM

INCREASED GLUCOSE TOLERANCE

1.
2. 3. 4. 5.

HYPOPITUITARISM HYPERINSULINISM HYPOTHYROIDISM ADRENAL CORTICAL HYPOFUNCTION DECREASED ABSORPTION SUCH AS SPRUE, COELIAC DISEASE.

DIAGNOSTIC CRITERIA FOR DM # FASTING PLASMA GLU. CONC. ON ONE OR MORE THAN ONE OCCASION >126 mg/dl. # 2 HRS. POST LOAD PLASMA GLUCOSE CONCENTRATION >200mg/dl. # SYMPTOMS OF DM WITH RANDOM PLASMA GLUCOSE CONCENTRATION >200mg/dl. IMPAIRED FASTING GLUCOSE # FASTING PLASMA GLUC. BETWEEN 110125mg/dl.

IMPAIRED GLUCOSE TOLERANCE # FASTING PLASMA GLUCOSE >126 mg/dl. #2 HR PLASMA GLUCOSE >140-199mg/dl. CAREFULL FOLLOW UP AS 2 % PROGRESS TO FRANK DIABETES.

MINI GTT
# FASTING & 2HR. POST GLUCOSE LOAD SAMPLES ARE TAKEN. SUFFICIENT FOR CORRECT ASSESMENT OF PT.

CORTICOSTERONE STRESSED GTT # 2 DOSES OF 50 mg CORTISONE ORALLY. # FIRST DOSE 8 HRS BEFORE GTT & SECOND 2 HRS BEFORE GTT. # GLUCOSE LOAD GIVEN ORALLY AS USUAL. # PLASMA GLUC. CONC. AT 1 HR>180 mg/dl & AT 2 HRS.>160 mg/dl. # HIGH VALUES SEEN IN PRE DIABETIC STATE, LATENT DIABETES & PERSONS PRONE TO GET DIABETES. # PREDNISOLONE AS 0.4mg/Kg BODY WT. CAN ALSO BE GIVEN.

EXTENDED GTT # GTT IS DONE NORMALLY UPTO 2 HRS & THEREAFTER IT IS EXTENDED FOR 4-5 HRS # INDICATIONS 1. TO DIFFERENTIATE BETWEEN HYPOGLYCEMIA DUE TO INSULIN SECRETING TUMORS OF PANCREAS & OTHER ENDOCRINAL CONDITIONS. 2. DONE IN PTS WITH POSTPRANDIAL HYPOGLYCEMIA DUE TO PARTIAL GASTRECTOMY.

FACTORS AFFECTING ORAL GTT

PATIENT PREPARATION - DURATION OF FAST

PRIOR CARBOHYDRATE INTAKE MEDICATIONS TRAUMA & ILLNESS INSULIN LEVELS AGE ACTIVITY WEIGHT

2.

ADMINISTRATION OF GLUCOSE - FORM OF GLUCOSE

- QUANTITY OF GLUCOSE INGESTED - VOLUME IN WHICH ADMINISTRATED - RATE OF INGESTION

3.

DURING THE TEST

POSTURE ANXIETY CAFFIENE & SMOKING PHYSICAL ACTIVITY TIME OF THE DAY

INTRAVENOUS GTT INDICATIONS 1. SUSPECTED MALABSORPTION 2. ALTERED GASTRIC PHYSIOLOGY 3. UNABLE TO TOLERATE GLUCOSE LOAD 4. MEASUREMENT OF FIRST PHASE INSULIN RESPONSE 5. HYPOTHYROIDISM

PREPARATION SAME AS THAT FOR ORAL GTT

PROCEDURE - 0.5 g/Kg BODY WT. TO A MAX OF 35 g. - DOSE IS ADM I/V OVER 3 min +/- 15 s. - BLOOD SAMPLES ARE TAKEN EVERY 10 min AFTER MID INJ TIME FOR 1 HR.

INTERPRATATION 1. PEAK VALUE OF BLOOD GLUCOSE 200-250 mg/dl REACHES WITHIN FEW MINUTES. 2. REACHES BACK TO 100 mg/dl BY 45-60 min. 3. ALL NORMAL CASES REQUIRE LESS THAN 60 min TO RETURN TO NORMAL BLOOD GLUCOSE LEVEL. 4. IN D.M IT TAKES MORE THAN 120 MINS TO RETURN TO NORMAL LEVELS.

BOTH OGTT & IVGTT HAVE POOR REPRODUCIBILITY & DECLINES WITH AGE.

GTT IN PREGNANCY

NORMAL PREGNANCY IS A/W INCREASED INSULIN RESISTANCE MORE SO IN 2nd & 3rd TRIMESTER OF PREGNANCY. EUGLYCEMIA IS MAINTAINED BY INCREASED INSULIN SECRETION. GDM DEVELOPS ONLY IN THOSE FEMALES WHO FAIL TO AUGMENT INSULIN SECRETION.

INTERNATIONAL CONFERENCE ON GDM HAS DIVIDED THE CANDIDATES DURING PREGNANCY INTO THREE CATEGORIES.

LOW RISK PATIENTS

1. 2.

3.
4. 5.

AGE LESS THAN 25 YEARS. NORMAL WEIGHT BEFORE PREGNANCY. NO FAMILY HISTORY OF DM. NO H/O ABNORMAL GTT. NO H/O POOR OBSTETRIC OUTCOME. AVERAGE RISK PATIENTS

1.

PTS. FALLING BETWEEN LOW & HIGH RISK GROUPS.

HIGH RISK PATIENTS

1. 2.

3.
4. 5.

MARKED OBESITY. GLYCOSURIA. STRONG FAMILY H/O DM. H/O GESTATIONAL DM IN PREVIOUS PREGNANCY. BIRTH WT. OF PREVIOUS BABY- MORE THAN 4 Kg.

GLUCOSE TESTS IN PREG

GCST GTT

GLUCOSE CHALLENGE SCREENING TEST (GCST) - PERFORMED AT 24-28 WK OF GESTATION ON ALL AVERAGE & HIGH RISK PTS. - 50 g ORAL GLUCOSE IS GIVEN. - MEASURE PLASMA GLU >140mg/d. PERFORM GTT GTT ` FASTING OF 8-14 HRS. MEASURE PLASMA GLU FASTING LEVEL. GIVE 75/100 mg OF GLUCOSE ORALLY. MEASURE PLASMA GLU HOURLY FOR 3 H

INTERPRATATION OF GTT IN PREGNANCY

GLU LOAD FASTING 1HR 2 HR 3 HR 100g 95 180 155 140 75g 95mg/dl 180 I55 -

#AT LEAST TWO VALUES MUST MEET OR EXCEED THESE VALUES. # IF RESULTS ARE NORMAL IN CLINICAL SUSPECT PATIENTS, REPEAT IN THIRD TRI.

IMPORTANCE OF GTT IN PREGNANCY

1 GDM OF PREG FEMALE IN IS A/W INCREASED INCIDENCE OF HYPOCALCEMIA, HYPOGLYCEMIA & MACROSMIA IN NEWBORN & THEREFORE A/W INCREASED MORBIDITY & MORTALITY.RECOGNITION BY GTT CAN AVERT THIS BY APPROPRIATE MANAGEMENT. 2. GDM IN PREGNANT FEMALES IS A/W INCREASED INCIDENCE OF C S & SUBSEQUENT RISK OF DEVELOPING TYPE 2 DM TO THE TUNE OF 40-70%; RISK MORE IN 1st 5 YEARS.

3.

WOMEN WITH GDM SHOULD BE EVALUATED AT 6 WEEKS AFTER THE DELIVERY IF NORMAL GLUCOSE VALUES, GLYCEMIA TO BE ASSESSED EVERY 3 YEARS.

COMA & ITS D/D

COMA A STATE FROM WHICH A PATIENT CAN NOT BE AROUSED BY ANY TYPE OF STIMULATION & NO PURPOSEFUL ATTEMPT IS MADE TO AVOID PAINFUL STIMULI. DIFFERENTIAL DIAGNOSIS OF COMA

DISEASES WITH NORMAL BRAINSTEM FUNCT

1. 2.

3.
4. 5.

INTOXICATIONS & HT ENCEPHALOPATHY METABOLIC DISORDERS & ECLAMPSIA SEVERE SYSTEMIC INFECTIONS POST SEIZURE STATE/ STATUS EPILEPTICUS SEVERE HYPER/HYPOTHERMIA

DISEASES CAUSING MENINGEAL IRRITATION

SAH ACUTE BACTERIAL MENINGITIS VIRAL ENCEPHALITIS FAT EMBOLISM MENINGEAL CARCINOMA

DISEASES WITH FOCAL CEREBRAL SIGN

BRAIN ABCESS SUBDURAL EMPYMA BRAIN TUMOR WITH OEDEMA HSV ENCEPHALITIS & VASCULITIS WITH INF HGE & INF WITH BRAINSTEM COMPRESSION

Diabetic ketoacidosis

KETOSIS ACCUMULATION OF KETONE BODIES IN BLOOD(KETONEMIA) & SUBSEQUENT EXCRETION IN URINE( KETONURIA) ACETOACETATE B-HYDROXY BUTYRATE ACETONE

CAUSES OF KETOSIS
1.
2. 3.

ALCOHOL CONSUMPTION STARVATION PROLONGED VOMITING

4.

5.
6. 7. 8. 9.

DM VON GIERKE HYPEREMESIS GRAVIDARUM PROLONGED LABOR HIGH FAT & LOW CARBOHYDRATE DIET SALICYLATE POISONING

1.

INSULIN DEF ACTIVATED LIPOLYSIS INCREASED FFA

INCREASED HEPATIC FA

ACCELERATED KETOGENESIS

2.

GLUCAGON EXCESS

INCREASED HEPATIC CARNITINE CONTENT DECREASED MALONOYL CoA CONTENT ACTIVATION OF ACYL TRANSFERASE ACCELERATED KETOGENESIS

3.

INCREASED ALCOHOL INTAKE

INCREASED NADH:NAD RATIO DECREASED PYRUVATE DECREASED OXALOACETATE ACCUMULATION OF ACETYL CoA KETOGENESIS

INCREASED GLUCAGON DECREASED INSULIN INCREASED GLUCONEOGENESIS DECREASED OXALOACETATE

INCREASED ACETYL CoA

ACCELERATED KETOGENESIS

DKA

IT IS AN ACUTE COMPLICATION OF D.M (T1>T2), CHARACTERIZED BY HYPERGLYCEMIA (MAY NOT BE EXCESSIVE), KETOSIS (ACIDOSIS), KETONURIA, ELECTROLYTE DISTURBANCE, DEHYDRATION AND HYPEROSMOLALITY LEADING TO HIGH MORBIDITY OR EVEN MORTALITY IF NOT URGENTLY TREATED.

S/S OF DIABETIC KETOACIDOSIS

1. 2. 3.

4.
5. 6.

FRUITY BREATH ODOUR DEHYDRATION HYPOTHERMIA KUSSUMUL BREATHING HYPOTENSION TACCHYCARDIA

ESSENTIALS OF DIAGNOSIS HYPERGLYCEMIA > 250 MG/DL. ACIDOSIS WITH BLOOD PH < 7.3. SERUM BICARBONATE < 15 MEQ/L. SERUM & URINE ARE POSITIVE FOR SUGAR & KETONES.

P.H. of DM Polyuria, Polydipsia & weakness. Anorexia, N & V. Ileus (hypo-K) Kaussumaul respiration = air hunger & acetone odor. Coma in 10% Hypothermia--- fever= infection Tacchycardia, hypotension, dehydration Hypotonia, hyporeflexia (hypo-K). ALL THE MANIFESTATIONS ARE IN ADDITION TO THE PREVIOUSLY DESCRIBED ESSENTIALS.

MANIFESTATIONS OF DKA

DETECTION OF KETONE BODIES

1.

DETECTION OF K B BY ACETEST - ACETEST TABS CONTAIN GLYCINE, SOD NITROPRUSSIDE, DISOD PHOS & LACTOSE. - ACETOACETATE OR ACETONE FORMS LAVENDER COLOR COMPLEX WITH NITROPRUSSIDE. - B-HYDROXY BUTYRATE DOES NOT REACT WITH NITROPRUSSIDE. - DISAOD PHOS PROVIDES OPTIMUM Ph

DETECTION BY KETOSTIX - MODIFICATION OF NITROPRUSSIDE TEST. - REAGENT STRIP IS USED INSTEAD OF TAB - GIVES + RXN IN 15s WITH A SPECIMEN .CONTAINING 50 mg OF ACETOACETATE/L - ACCOMPANYING COLOR CHART GIVES READINGS FOR KETONE CONC. ACCORDING TO THE COLOR OF THE KETOSTIX. 3. DETERMINATION OF B-HYDROXYBUTYRATE B-HYDROXYBUTYRATE ACETOACETATE
2.

NAD

NADH+H

NADH + NBT NAD + RED NBT # ABSORBACE OF RED NBT(COLORED COMPLEX) IS READ.
4.

DETERMINATION OF K B IN URINE BY USE OF ACETEST & KETOSTIX

IN HEALTH SERUM B-HYDROXY BUTYRATE VALUES USUALLY RANGE FROM 0.21-2.81 mg/dl. IN DIABETIC KETOACIDOSIS THESE ARE MORE THAN 20mg/dl.

Goals of therapy
Rehydration Euglycemia Correction of acid-base Correction of electrolyte imbalance. Investigate the PPT. factor.

Priorities for TTT: 1st priority is rehydration 2nd is Insulin 3rd is K

Average losses in D.K.A:

WATER60-100ml.kg K Cl P Na

(6L)

4-6mEq/kg (350 m mol) 5-13mEq/kg (500 m mol) 3-9mEq/kg (400 m mol)

2-5 mEq/kg
0.5-1.5 mEq/kg

Mg

HYPERGLYCEMIC HYPEROSMOLAR STATE

(hyperglycemic, hyperosmolar, nonketotic coma)

Essentials of Diagnosis
Severe

mg/dL. Hyperosmolality > 310 mosm/kg. No acidosis; blood pH above 7.3. Serum bicarbonate > 15 meq/L. Normal anion gap (< 14 meq/L). Severe dehydration

hyperglycemia > 600

 The second most common form of hyperglycemic

coma.

It occurs in patients with mild or occult diabetes (T2)

Weakness, polyuria, and polydipsia.

(no acidosis) may lead to thrombotic complications.

Profound dehydration without Kussmaul respirations

Severe hyperosmolality causes mental confusion

progressing to convulsions and deep coma (> 320-33 mosm/kg). bad prognosis.

Underlying renal insufficiency or CHF

A precipitating event such as infection, AMI, CVS, or

recent operation & peritoneal dialysis (glucose

Management
ADEQUATE REHYRATION INSULIN THERAPY POTTASIUM SUPPLEMENTATION

Complications:
The leading cause of DKA mortality is cerebral edema Hypokalemia is a complication that is precipitated by failing to rapidly address the total body potassium deficit brought out by rehydration

Complications:
Hypoglycemia may result from inadequate monitoring of glucose levels during insulin therapy. Acute pulmonary edema potentially is related to aggressive or excessive fluid therapy.

Other complications
MI
Acute

gastric dilatation Erosive gastritis Late hypoglycemia Respiratory distress Infection

HYPEROSMOLAR COMA

Sever

Hyperglycemia > 600 mg/dL. Hyperosmolality > 310 mosm/kg. No acidosis; blood pH above 7.3. Serum bicarbonate > 15 meq/L. Normal anion gap (< 14 meq/L). Severe dehydration

HYPEROSMOLAR COMA
1.

PATHOPHYSIOLOGY DIFFERENT FROM DKA: NO KETOGENESIS (USUALLY IN TYPE 2 ELDERLY PATIENTS WHO MAY HAVE ENOUGH INSULIN TO INHIBIT FFA RELEASE) 2. PROFOUND DEHYDRATION IS THE MAIN ISSUE 3. MORE PRONE TO THROMBOEMBOLISM AND CEREBRAL EDEMA

PATHOGENESIS OF HOC
PARTIAL OR RELATIVE INSULIN DEF DEC GLU UTILIZATION INC HEPATIC GLU OUTPUT MASSIVE GLYCOSURIA WITH WATER LOSS CONTRACTION OF PLASMA VOL DEVELOPMENT OF RENAL IN SUFFICIENCY

LIMITATION OF RENAL GLU LOSS

INC BLOOD GLU CONC SEVERE HYPEROSMOLARITY MENTAL CONFUSION/ COMA

MORTALITY RATE IN HOC IS VERY HIGH. REQUIRES URGENY TREATMENT.

TREATMENT
I/V FLUID. INSULIN. POTTASIUM SUPPLEMENTATION. SOD BICARBONATE IF LACTIC ACIDOSIS ANTIBIOTICS

Lactic acidosis

1. 2.

3.
4.

5.
6.

7.

MOST COMMON TYPE OF METABOLIC ACIDOSIS. ACCUMULATION OF EXCESS LACTIC ACID IN THE BODY. SOURCES OF LACTATE BEING RBC, BRAIN, SKIN, RENAL MEDULLA, & SK. MUSCLE. IT IS METABOLISED BY LIVER & KIDNEY. NORMAL CONC. IS 1 mmol/l. DURING STENTUOUS EXERCISE LACTATE PRODUCTION INCREASES TO 20 mmol/l. LACTATE CONC. EXCEEDING 5mmol/l & PH <7.25 INDICATE SIGNIFICANT LACTIC ACIDOSIS.

CAUSES OF LACTIC ACIDOSIS HYPOXIC METABOLIC

HYPOXIC
1. 2.

A/W DECREASED TISSUE OXIGENATION. COMMONLY SEEN IN SHOCK HYPOVOLEMIA LVF & MI SEVERE ANEMIA CO & CYANIDE POISONING

METABOLIC
A/W METABOLIC CAUSES 2. SEEN IN DM KETOACIDOSIS LIVER FAILURE INFECTIONS LYMPHOMAS LEUKEMIAS 3. DRUGS ETHANOL
1.

4.

5.

SALICYLATES PHENPHORMIN METFORMIN SOD NITROPRUSSIDE ETHYLELE GLYCOL NUCLEOSIDE REVERSE TRANS CRIPTASE INHIB JEJUNAL BYPASS ( D LACTIC ACIDOSIS) INBORN ERRORS OF METABOLISM G6PD FI6 BIS PHOPHATASE PYRUVATE CARBOXYLASE PDH FA OXIDATION DEFECTS

6.

INCRESED CSF LACTATE CONC. CVA BACTERIAL MENINGITIS EPILEPSY INTRA CRANIAL HGE

Essentials of Diagnosis

Severe acidosis with hyperventilation. Blood pH below 7.30. Serum bicarbonate < 15 meq/L. Anion gap > 15 meq/L. Absent serum ketones. Serum lactate > 5 mmol/L

DETECTION OF LACTATE 1. L-LACTATE LDH PYRUVATE

NAD NADH + H #THE EQ OF THE RXN LIES TO THE LEFT WHICH IS MADE TOWARDS RIGHT BY MAINTAINING THE PH OF RXN AT 9.0-9.6, PROVIDING EXCESS NAD & REMOVING PYRUVATE BY REACTING IT WITH L- GLUTAMATE BY ENZYME ALT.

# NADH MEASURED AT 340 nm BY SPECTROPHOTOMETER

2.

L-LACTATE+ O2 PYRUVATE +H2O2 H2O2 + 4-AMINOANTIPYRIN + 1,7-DIHYDRONAPHTHALENE PEROXIDASE

RED DYE #ABSORBANCE OF THE DYE COMPLEX IS MEASURED AT 540 nm.

3. 4.

GAS CHROMATOGRAPHY PHOTOMETRY THE ENZYMATIC METHODS ARE METHODS OF CHOICE.

Management

TREATING THE PRECIPITATING CAUSE.

ADEQUATE OXYGENATION & VASCULAR PERFUSION.

EMPIRICAL ANTIBIOTIC COVERAGE FOR SEPSIS. ALKALINIZATION WITH IV SODIUM BICARBONATE TO KEEP THE PH ABOVE 7.2.

HEMODIALYSIS MAY BE USEFUL IN CASES WHERE LARGE SODIUM LOADS ARE POORLY TOLERATED.