RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES

BANGALORE, KARNATAKA.

ANNEXURE –II

PROFORMA FOR REGISTRATION OF SUBJECT FOR DISSERTATION

1. / NAME OF THE
CANDIDATE / DR. SONALI APPAIAH
ADDRESS / ROOM NO.18, PG HOSTEL, BMC & RI, BANGALORE-560002.
2. / NAME OF THE INSTITUTION / BANGALORE MEDICAL COLLEGE AND RESEARCH INSTITUTE, BANGALORE.
3. / COURSE OF
STUDY AND
SUBJECT / MD GENERAL MEDICINE
4. / DATE OF
ADMISSION / 31ST MAY 2011
5. / TITLE OF THE TOPIC / A STUDY OF PHOSPHOROUS LEVELS AS A PROGNOSTIC INDICATOR IN DIABETIC KETOACIDOSIS .
6. / BRIEF RESUME OF THE INTENDED WORK
6.1. NEED FOR STUDY:
Phosphorus is an essential element. Phosphorus-containing compounds have important roles in cell structure (cell membrane and nucleic acids), cellular metabolism (generation of ATP), regulation of sub cellular processes (phosphorylation of key enzymes), and maintenance of acid–base homeostasis (urinary buffering).Hypophosphatemia occurs in 1% to 5% of all hospitalized patients. This prevalence increases to between 20% and 40% in adult patients with diabeticketoacidosis.
Phosphate depletion is common in diabetic ketoacidosis Intracellular phosphate is lost as a result of acidosis, and renal phosphate excretion is increased. During treatment with insulin, phosphate is taken up intracellularly with resultant hypophosphatemia. Hypophosphatemia is associated with a number of clinical sequelae, including decreased cardiac output, respiratory muscle weakness, rhabdomyolysis, central nervous system depression, seizures and coma, acute renal failure, and hemolysis.(9)
In the setting of DKA, phosphate losses average 3 to 7 mmol/kg. Complications of hypophosphatemia generally occur at serum levels below 1.0 mg/dL. Phosphate repletion should be used in patients with serum phosphate. levels below 1.0 mg/dL and in patients with evidence of cardiac or respiratory compromise, hypoxia, or hemolytic anemia.(10)
Early recognition and treatment of severe hypophosphatemia in the treatment of diabetic ketoacidosis is important to reduce the morbidity and mortality associated with diabeticketoacidosis. Hence phosphorous acts as a prognostic indicator in diabetic ketoacidosis.
6.2. REVIEW OF LITERATURE:
Reilly et al(1) found certain populations are likely to include a greator proportion of hypophosphatemic patients – for example , alcoholics(0.9%), septic patients(2.4%), malnourished patients(10.4%), and patients with diabetic ketoacidosis(14.6%). In a retrospective study ,severe hypophosphatemia was associated with fourfold increase in mortality.
David W Miller et al(2) showed that hyophosphatemia may be seen in anywhere from 20% to 80% of patients who present to emergency department with alocoholic emergencies, diabetic ketoacidosis, and sepsis.
Liu PY et al(3) found that in critically ill patient, the symptoms of hypophosphatemia are not apparent and may mimic the symptoms of other underlying disease. Although phosphate replacement is not recommended routinely in diabetic ketoacidosis, if the patient develops cardiopulmonary distress, anemia or severe hypophosphatemia, phosphate therapy under close surveillance is indicated.
Akinori Osuka et al(4) suggested frequent monitoring of serum phosphate and phosphate replacement for patients with diabetic ketoacidosis and severe hypertriglyceridemia.
Brasil de Oliveira Iglesias S et al(5) showed that, early recognition and treatment of severe hypophosphatemia in the treatment of diabetic ketoacidosis are important to reduce the risk of neurological complications.
Megarbane et al(6) reported hypophosphatemia-related, life-threatening encephalopathy in a case with severe ketoacidosis. No other cause of encephalopathy was found. Prompt phosphate repletion resulted in progressive and complete recovery.
Alev Oguz Kutlu et al(7) reported rhabdomyolysis due to severe hypophosphatemia, where the level of serum phosphorus was observed to be as low as 0.42 mg/dL on the 16th hour of ketoacidosis treatment.
Shilo S et al(8) found that hypophosphatemia in diabetic ketoacidosis is well recognized, but is believed to be usually of moderate severity. Our experience indicates that severe hypophosphatemia requiring phosphate supplementation does occur in diabetic patients, and calls for increased awareness for the clinical and laboratory manifestations of this complication of diabetic ketoacidosis.
6.3. AIMS AND OBJECTIVES OF THE STUDY:
The study of phosphorous levels as a prognostic indicator in diabetic ketoacidosis.
7.0 / MATERIALS AND METHODS
7.1. SOURCE OF DATA:
The study will be conducted on 50 individuals with diabetic ketoacidosis, at Victoria Hospital and Bowring and Lady Curzon Hospital attached to Bangalore Medical College and Research Institute, Bangalore.
7.2. METHOD OF COLLECTION OF DATA:
A. STUDY DESIGN
Cross-sectional study
B.  STUDY PERIOD
November 2011 to May 2013
C.  PLACE OF STUDY
Victoria Hospital and Bowring and Lady Curzon Hospital attached to Bangalore Medical College and Research Institute, Bangalore.
D.  SAMPLE SIZE.
A minimum of 50 patients with diabetic ketoacidosis will be studied .
E.  INCLUSION CRITERIA.
1.Patients who have given written informed consent.
2.Patients with diabetic ketoacidosis.
3.Patients with Type 1 & 2 diabetes mellitus.
4. Patients who are >18yrs age.
F.  EXCLUSION CRITERIA.
1.Patients who have not given written informed consent.
2.Patients with malnutrition , malabsorption syndromes.
3. Patients on diuretics ,steroids , phosphate binding antacids.
4.Patients with renal transplantation.
5.Patients with hyperparathyroidism.
6.Patients with pancreatitis, burns ,volume expansion.
7.Patients who are alcoholics.
8.Respiratory alkalosis – hyperventilation, panic attacks, salicylate poisoning
9.Rapid cellular uptake – refeeding syndrome, leukemic blast cell crises, hungry bone syndrome.
G.  STATISTICAL ANALYSIS.
Depending upon the data available appropriate statistical test will be applied qualitatively by chi-square and quantitatively by t- test.
H.  METHODOLOGY.
Phosphorous levels will be estimated on day one, after 48 hours of admission or worsening of patient’s condition and at discharge. It will be correlated to prognosis of patient in diabetic ketoacidosis.
.
7.3. DOES THE STUDY REQUIRE ANY INVESTIGATIONS OR INTERVENTIONS TO BE CONDUCTED ON PATIENTS OR OTHER HUMANS OR ANIMALS? IF SO, PLEASE DESCRIBE BRIEFLY.
Yes. It involves following tests on human subjects.
INVESTIGATIONS REQUIRED:
a.Random Blood Sugar.
b.Arterial Blood Gas (ABG)-Arterial Ph .
-Arterial PCO2.
-Serum bicarbonate.
c. Plasma and urine ketone Bodies .
d.Complete blood counts.
e. Renal function tests.
f. Liver function test.
g.Serum electrolytes
·  Phosphorous
·  Calcium
·  Magnesium
·  Potassium
·  Sodium
·  Chloride.
7.4. HAS THE ETHICAL CLEARANCE BEEN OBTAINED FROM YOUR INSTITUTION IN CASE OF 7.3
YES
8. / LIST OF REFERENCES:
1.  Amanzadeh J and Reilly RF Jr, “Hypophosphatemia: an evidence-based approach to its clinical consequences and management.” Nature Clinical Practice Nephrology 2006;2:136-148
2.  Miller DW, Slovis CM, “Hypophosphatemia in the emergency department therapeutics”. American Journal of Emergency Medicine 2000 july;18: 457-461.
3.  Liu PY, Jeng CY , “Severe hypophosphatemia in a patient with diabetic ketoacidosis and acute respiratory failure”. J Chin Med Assoc 2004 Jul;67(7):355-359
4.  Osuka A , Matsuoka T and Idoguchi K, “Hypophosphatemia and Resulting Cardiac Arrest during the Treatment of DiabeticKetoacidosis with Hypertriglyceridemia”. Inter Med 2009; 48: 1391-1395.
5.  Brasil de Oliveira Iglesias S, Leite PH , Brunow de CarvalhoW,“Study of Hypophosphatemia-Induced Seizure in a Patient With Diabetic Ketoacidosis”. Pediatr Emer Care 2009;25: 859-861
6.  Megarbane B , Guerrier G, Blancher A, Meas T, Guillaussaeu PJ, Baud FJ, “A possible hypophosphatemia-induced, life-threatening encephalopathy in diabetic ketoacidosis: a case report.” Am J Med Sci 2007 Jun;333(6):384-6.
7.  Kutlu A O, Kara C, Cetinkaya S, “Rhabdomyolysis without detectable myoglobulinuria due to severe hypophosphatemia in diabetic ketoacidosis.” Pediatric Emergency Care 2011;27(6):537-538
8.  Shilo S , Werner D, Hershko C, “Acute hemolytic anemia caused by severe hypophosphatemia in diabetic ketoacidosi.”.Acta Haematologica 1985;73:55-57
9.  Wyckoff J, Abrahamson MJ.Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State. C Roland Kahn, Gordan C Wies, George L.King, Alen M Jacobson, Alene Moses, Robert J Smith. JOSLINS DIABETES MELLITUS, 14th Edition Lippincott Williams 2008;53:892-896.
10.  Inzucchi S E,Sherwin R E . Type 1 Diabetes Mellitus. Goldman L, Ausiello D, Arend , Amitage, Clemmons, Drazen, Griggs, Landry, Levinson, Rustgi, Scheld. GOLDMANS CECIL MEDICINE 24th Edition Elsevier 2008;236:1691-1694
9. / SIGNATURE OF THE CANDIDATE: / DR. SONALI APPAIAH
10. / REMARKS OF THE GUIDE
·  Diabetic ketoacidosis is a life-threatening emergency which occurs in patients with uncontrolled diabetes mellitus.
·  Phosphorous depletion is common in diabetic ketoacidosis and moderate to severe hypophosphatemia is associated with increased morbidity and mortality.
·  Serum phosphorous level estimation is a simple and cost-effective procedure. Hence this study is being taken to assess the significance of serum phosphorous level in prognosis of diabetic ketoacidosis.
11. / NAME AND DESIGNATION
11.1.GUIDE:
11.2. SIGNATURE: / PROF.DR. ANANDA KUMAR M, MD
PROFESSOR, DEPT OF MEDICINE,
BANGALORE MEDICAL COLLEGE AND RESEARCH INSTITUTE, BANGALORE.
11.5.HEAD OF THE DEPARTMENT:
11.6. SIGNATURE: / PROF.DR. PRABHAKAR.B, MD
PROFESSOR AND HEAD
DEPARTMENT OF MEDICINE
BANGALORE MEDICAL COLLEGE &
RESEARCH INSTITUTE, BANGALORE.
12.1.) DEAN AND DIRECTOR OF BANGALORE MEDICAL COLLEGE AND RESEARCH INSTITUTE:
12.2.)REMARKS OF DEAN AND DIRECTOR:
12.3.) SIGNATURE : / PROF.DR.O.S.SIDDAPPA, DEAN AND DIRECTOR OF BANGALORE MEDICAL COLLEGE AND RESEARCH INSTITUTE
ANNEXURE-I
INFORMED CONSENT
I, Mr. /Mrs. /Ms have been explained in a language well understood by me to my satisfaction about the study being carried out. I exercise my own free will power of choice and hereby give consent for myself being used as an object of, “A STUDY OF PHOSPHOROUS LEVELS AS A PROGNOSTIC INDICATOR IN DIABETIC KETOACIDOSIS” conducted by Dr. Sonali Appaiah , Department of General Medicine , Victoria hospital/ Bowring and Lady Curzon hospital, Bangalore Medical College and Research Institute.
The attending doctors have informed me about the purpose of study, the materials to be used during the course of the study as well as the complications associated with the methods/ tools to be used. I shall not hold the doctors or the staff responsible for any untoward consequences. I have no issues about sharing my details in case records and would co-operate for the study.I have been informed that I will not be sharing any incentives.
I am also aware of my right to opt out of the study without prejudice to further treatment at any time during the course of study without having to give any reasons to do so. During the discussion with treating doctor at any time, there would be no compulsion to furnish any details and hence, the willingness to take part in the study is completely voluntary.
Signature of Doctor: Signature/ Left thumb
Date: impression of the Patient
Signature of the witness:
Date: