Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 12

Table of Contents

ABSTRACT................................................................................................................................................3
CHAPTER ONE: INTRODUCTION..........................................................................................................4
1.1: Background......................................................................................................................................4
1.2: Problem statement............................................................................................................................5
1.3: Rationale of the study.......................................................................................................................6
1.4: Research question.............................................................................................................................6
1.5: objectives..........................................................................................................................................6
1.5.1Broad objective............................................................................................................................6
1.5.2 Specific objectives......................................................................................................................6
CHAPTER TWO: LITERATURE REVIEW..............................................................................................6
2.1: introduction......................................................................................................................................6
2.2: Pathophysiology of DKA.................................................................................................................7
2.3: Causes of DKA.................................................................................................................................7
2.4: Diagnosis..........................................................................................................................................8
2.5: Treatment of DKA............................................................................................................................8
CHAPTER THREE: RESEARCH METHODOLOGY...........................................................................................11
3.1 Study area........................................................................................................................................11
3.2 study design.....................................................................................................................................11
3.3 study population..............................................................................................................................11
3.4 selection criteria...............................................................................................................................11
3.4.1 Inclusion criteria.......................................................................................................................11
3.4.2 Exclusion criteria......................................................................................................................11
3.5 sampling procedure..........................................................................................................................11
3.6 sample size estimation.....................................................................................................................11
ABSTRACT

Background: Diabetic ketoacidosis (DKA) is the consequence of absolute or relative insulin

deficiency and concomitant elevation of counter regulatory hormones resulting in

hyperglycemia, metabolic acidosis, ketosis and varying degrees of dehydration. This condition is

life-threatening despite improvements in diabetic care.

Objective: To determine factors associated with mortality in DKA patients admitted at TRRH

Intensive care unit.

Methods: This was retrospective study in which records of 21 patients with the diagnosis of

DKA admitted in ICU from January 2022 to December 2022 was reviewed.

Results: The overall mortality rate was 28.5%. Delayed diagnosis, renal failure, severe malaria,

deep venous thrombus (DVT), septicemia and presence of other complications were the major

risk factors associated with mortality in DKA patients admitted at TRRH intensive care unit.

Delayed diagnosis was 16.6%,renal failure 33.3%, severe malaria16.6%,DVT 16.6% and

septicemia 50% .

Conclusion: Considering the mortality rate obtained in the study there is an urgent need of

creating awareness among people especially DM patients in their clinics to avoid delay care

seeking behaviors so as to decrease mortality caused by DKA.since there was a significant

relationship between septicemia and severity of outcome in DKA patients health care providers

should focus on early organ failure assessment by using QSOFAS and manage sepsis as per

protocol.
CHAPTER ONE: INTRODUCTION

1.1: Background

Diabetic ketoacidosis (DKA) is serious and potentially life-threatening complication of diabetes

mellitus and it is characterized by hyperglycemia, pH lower than 7.3 and dehydration[1, 2].

Mortality of DKA varies across the world[3]. In USA, DKA account for about 0.4% mortality

rate[3].Mortality in DKA among people has been reported to be 0.3% and 13.4% in developed

and developing countries respectively(citation). In India it was reported that Hospital mortality

from DKA case is high as 30%[2].

A study done in Australia reported that DKA mortality rates range from 2 to 40% depending on

the region[4]. It was reported that Sex, baseline biochemical parameters such as APACHE II

score, and phosphate level were important predictors of the DKA-associated mortality in DKA

patients[2]
1.2: Problem statement

Despite improvement in diabetic care, DKA remain the leading cause of hospitalization in

developed and developing countries[5].

DKA warrants immediate and aggressive intervention. even with appropriate interventions DKA

is associated significant morbidity and possible mortality in diabetic patients ,therefore proper

diagnosis, and management of DKA and its causes is a key factor towards reducing mortality

caused by DKA .Therefore this study intend to assess factors leading to high mortality in DKA

patients admitted in ICU.


1.3: Rationale of the study

The findings of this study will help Tanga referral regional hospital to came up with strategies that will
reduce mortality in DKA patients.

1.4: Research question

What are the factors associated with high mortality in DKA patients admitted at TRRH intensive

care unit.

1.5: objectives

1.5.1Broad objective

To determine associated with mortality in DKA patients admitted at TRRH Intensive care unit.

1.5.2 Specific objectives


CHAPTER TWO: LITERATURE REVIEW

2.1: introduction

Diabetic ketoacidosis(DKA) is a life-threatening but preventable complication of diabetes

characterized by uncontrollable hyperglycemia(>250mg/dl), metabolic acidosis and increased

ketenes concentration that occurs most frequently in people with type 1 diabetes[6].

DKA occurs most common as a result of absolute or relative insulin deficiency and remains one

of the most frequent cause of death in people with type 1 diabetes. Whilst DKA occurs most

frequently in those with type 1 diabetes, it can occur in people with type 2 diabetes or gestational

diabetes[7].

2.2: Pathophysiology of DKA

Depending on the concentration of circulating insulin, at very lowest concentration insulin

inhibits lipolysis and this switches off ketones production. Higher insulin concentration

stimulates glucose uptake into the cells, inhibits glycogenolysis and stimulates glycogen

synthesis[8].Thus if insulin is absent or concentration of counter-regulatory hormones –

cortisol,catecolamines or glucagon are high, such as at times of acute illness, then insulin

mediated cellular glucose uptake is reduced, necessitating the provision of an alternative energy

substance. Insulin deficiency cause an increase in activity of hormone sensitive lipase. This leads

to triglyceride breakdown and free fatty acid liberation[9].These free fatty acid form acetyl

coenzyme A (CoA) due to beta oxidation, and enter tricarboxylic acid (TCA) cycle.However,

when there is high concentration of free fatty acid as with insulin deficient states, the TCA cycle

is overwhelmed and the acetyl CoA is instead converted to ketone bodies in the liver [10]. These
ketone bodies enter the circulation primarily as beta-hydroxybutyrate and acetoacetone at 10:1

ration[11].

Accumulation of those ketone bodies result in high anion gap metabolic acidosis seen in DKA ,

but it is important to ensure than the high anion gap is not due to other causes of fixed acid

retention like aspirin overdose, renal failure and ketoacidosis from other causes like liver disease.

2.3: Causes of DKA

The most common DKA causes are infection, poor adherence to prescribed medications and

Intercurrent illness, fragmentation of care, presence of co-morbidities such as end stage renal

failure[12]. Majority of DKA cases are precipitated by infection which have high incidence rate

especially in developing countries[7].

2.4: Diagnosis

Diagnosis of DKA require all three components to be presents which are D – means that the

individual must have hyperglycemia(RBG>11mmo/l) at time of presentation or have been

previously diagnosed with diabetes, The ‘K’means they must have urine ketone 2+ on standard

urine ketone stick and ‘A’ means they must have a pH <7.3 or a serum bicarbonate of <

15.0mmol/L[13] and adjusted for albumin anion gap of >12[14]. The diagnosis of DKA is

challenging in patients with concomitant underlying chronic metabolic acidosis or mixed acid-

base disorders like in people with chronic kidney disease stage 4-5 , Anion gap of >20 usually

supports the diagnosis of DKA in these patients[7, 14].


2.5: Treatment of DKA

Therapeutic goals of DKA management include optimization of volume status, hyperglycemia,

ketoacidosis, electrolyte abnormalities and potential precipitating factors. Majority of patients

with DKA present to the emergency department (EMD) and Intensive care unit (ICU).

Therefore, physicians should initiate the management of hyperglycemic crisis while a physical

examination is performed, basic metabolic parameters are obtained, and final diagnosis is made.

Several important steps should be followed in the early stages of DKA management:

1. collect blood for metabolic profile before initiation of intravenous fluids;

2. correction of dehydration /hypovolemia (over 48 hours)

3. correction of potassium

4. correction of acidosis/hyperglycemia

5. examine, investigate and treat the patient for potential precipitating factors

The protocol for the management of patients with DKA is presented in below It must be

emphasized that successful treatment requires frequent monitoring of clinical and metabolic

parameters that support resolution of DKA[14].


CHAPTER THREE: RESEARCH METHODOLOGY

3.1 Study area

This study was conducted at Tanga referral regional hospital, which is located in Tanga city

3.2 study design

The study was hospital based cross sectional study in which records of 21 patients with the diagnosis

of DKA admitted in ICU from January 2022 to December 2022 was reviewed.

3.3 study population

This study involves records of DKA patients admitted at TRRH intensive care unit from January

2022 to December 2022.

3.4 selection criteria

3.4.1 Inclusion criteria

Ward records of DKA patients admitted from January 2022 to December 2022

3.4.2 Exclusion criteria

DKA patients with missing data was not included in the study

3.5 sampling procedure

Simple random sampling was used in this study

3.6 sample size estimation


REFERENCE

1. Elkituni, A., et al., Profile of diabetic ketoacidosis at the National Diabetes and Endocrine Center
in Tripoli, Libya, 2015. Diabetes & Metabolic Syndrome: Clinical Research & Reviews, 2021.
15(3): p. 771-775.
2. Agarwal, A., et al., Prognostic factors in patients hospitalized with diabetic ketoacidosis.
Endocrinology and metabolism, 2016. 31(3): p. 424-432.
3. Dhatariya, K.K., Defining and characterising diabetic ketoacidosis in adults. Diabetes research
and clinical practice, 2019. 155: p. 107797.
4. Venkatesh, B., et al., Incidence and outcome of adults with diabetic ketoacidosis admitted to
ICUs in Australia and New Zealand. Critical Care, 2015. 19(1): p. 1-12.
5. Bismuth, E. and L. Laffel, Can we prevent diabetic ketoacidosis in children? Pediatric diabetes,
2007. 8: p. 24-33.
6. Nyenwe, E.A. and A.E. Kitabchi, The evolution of diabetic ketoacidosis: An update of its etiology,
pathogenesis and management. Metabolism, 2016. 65(4): p. 507-521.
7. Suwarto, S., et al., Predictors of five days mortality in diabetic ketoacidosis patients: a
prospective cohort study. Acta Medica Indonesiana, 2014. 46(1).
8. Barwell, N.D., G.A. McKay, and M. Fisher, Drugs for diabetes: Part 7 insulin. British Journal of
Cardiology, 2011. 18(5): p. 224.
9. Foster, D.W. and J.D. McGarry, The metabolic derangements and treatment of diabetic
ketoacidosis. New England Journal of Medicine, 1983. 309(3): p. 159-169.
10. Sato, Y., et al., Factors affecting in-hospital mortality of diabetic ketoacidosis patients: A
retrospective cohort study. Diabetes Research and Clinical Practice, 2021. 171: p. 108588.
11. Stentz, F.B., et al., Proinflammatory cytokines, markers of cardiovascular risks, oxidative stress,
and lipid peroxidation in patients with hyperglycemic crises. Diabetes, 2004. 53(8): p. 2079-2086.
12. Wang, Z., E. Kihl‐Selstam, and J.W. Eriksson, Ketoacidosis occurs in both Type 1 and Type 2
diabetes—a population‐based study from Northern Sweden. Diabetic medicine, 2008. 25(7): p.
867-870.
13. Savage, M., et al., Joint British Diabetes Societies guideline for the management of diabetic
ketoacidosis. Diabetic medicine: a journal of the British Diabetic Association, 2011. 28(5): p. 508-
515.
14. Gosmanov, A.R., E.O. Gosmanova, and E. Dillard-Cannon, Management of adult diabetic
ketoacidosis. Diabetes, metabolic syndrome and obesity: targets and therapy, 2014. 7: p. 255.

You might also like