’ Review

Comprehensive review of diabetic ketoacidosis:

an update
Chukwuka Elendu, MDa,*, Johnson A. David, MBBSi, Abasi-O. Udoyen, MBBSj, Emmanuel O. Egbunu, MBBSd,
Ifeanyichukwu C. Ogbuiyi-Chima, MBBSe, Lilian O. Unakalamba, MBBSf, Awotoye I. Temitope, MBBSg,
Jennifer O. Ibhiedu, MBBSe, Amos O. Ibhiedu, MBBSe, Promise U. Nwosu, MBBSh, Mercy O. Koroyin, MBBSk,
Chimuanya Eze, MBBSe, Adeyemo I. Boluwatife, MBBSd, Omotayo Alabi, MBBSc, Olisa S. Okabekwa, MBBSb,
John O. Fatoye, MBBSd, Habiba I. Ramon-Yusuf, MBBSl

Abstract
The most frequent hyperglycemic emergency and the leading cause of death in people with diabetes mellitus is diabetic ketoacidosis
(DKA). DKA is common in people with type 1 diabetes, while type 2 diabetes accounts for roughly one-third of occurrences.
Although DKA mortality rates have generally decreased to low levels, they are still significant in many underdeveloped nations. In
industrialized countries, its mortality rate ranges from 2 to 5%, but in underdeveloped nations, it ranges from 6 to 24%. Therefore, it is
always lethal if misdiagnosed or improperly treated. According to specific research, DKA can be present at the time of type 1
diabetes onset in 25 to 30% of cases and in 4 to 29% of young people with type 2 diabetes mellitus, and its features include
hyperglycemia, metabolic acidosis, and ketosis with its triggering factors commonly being infections, newly discovered diabetes,
and failure to start insulin therapy. Less than 20% of DKA patients present comatose, and patients with different levels of con-
sciousness can present at other times. A close association between abnormalities found during a mental status evaluation and
osmolality seems to exist. Hospital admission is necessary for vigorous intravenous fluid therapy, insulin therapy, electrolyte
replacement, diagnosis and treatment of the underlying triggers, and routine monitoring of the patient’s clinical and laboratory
conditions to manage DKA properly. Appropriate discharge plans should include actions to prevent a DKA recurrence and the
proper selection and administration of insulin regimens.
Keywords: diabetic ketoacidosis, hyperglycemia, insulin deficiency, ketones, type 1 diabetes

Introduction and background

HIGHLIGHTS
Diabetic ketoacidosis is a grievous complication of diabetes
• Diabetic ketoacidosis is the most frequent hyperglycemic
that occurs when there is a lack of insulin in the body,
emergency.
resulting in elevated blood glucose levels and the production of
• Diabetic ketoacidosis is the leading cause of death in people
ketones. Diabetic ketoacidosis is a medical emergency that
with diabetes mellitus.
requires immediate treatment, as it can lead to life-threatening • DKA is common in people with type 1 diabetes.
complications such as cerebral edema, acute respiratory dis-
tress syndrome, and sepsis[1]. It is becoming more prevalent
worldwide, particularly among type 1 diabetic children and
a b
Federal Medical Center, Owerri, University of Nigeria Teaching Hospital, Ituku
adolescents[1]. While insulin therapy and patient education
Ozalla, cRedeemer’s University, dUniversity of Ilorin Teaching Hospital, eBabcock have improved, diabetic ketoacidosis remains a common cause
University, fRivers State University Teaching Hospital, Portharcourt, gLagos of hospitalization and is associated with notable morbidity and
University Teaching Hospital, hAbia State University, Nigeria, iVN Karazin National
mortality[2,3]. Among the immediate treatment options for
University, Kharkiv, Ukraine, jPirogov Medical University, Rossijskij nacional’nyj
issledovatel’skij medicinskij universitet imeni N I Pirogova, Russia, kBromley severe diabetic ketoacidosis is a multidisciplinary approach
Healthcare and lUniversity Hospital Lewisham, UK that emphasizes correcting fluid and electrolyte imbalances,
Sponsorships or competing interests that may be relevant to content are disclosed at restoring insulin sensitivity, and preventing complications.
the end of this article. Primary care aims to prevent the progression of diabetic
*Corresponding author. Address: Federal Medical Center Owerri Imo State, Nigeria. ketoacidosis and minimize the risk of cerebral edema, a rare
Tel/fax.: + 2348134939606, E-mail: elenduchukwuka@yahoo.com (C. Elendu).
but potentially fatal complication[4,5]. A recent publication has
Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. This is an
shed light on the pathophysiology of diabetic ketoacidosis,
open access article distributed under the Creative Commons Attribution License 4.0
(CCBY), which permits unrestricted use, distribution, and reproduction in any including the role of insulin deficiency, altered glucose meta-
medium, provided the original work is properly cited. bolism, and acid-base disturbances[3]. Technological advances
Annals of Medicine & Surgery (2023) 85:2802–2807 and monitoring techniques have also allowed for more precise
Received 30 March 2023; Accepted 13 May 2023 management of fluid and electrolyte imbalances, insulin ther-
Published online 23 May 2023 apy, and other adjunctive therapies[5]. The management of
http://dx.doi.org/10.1097/MS9.0000000000000894 severe diabetic ketoacidosis is not without challenges. For

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example, insulin therapy can rapidly drop blood glucose levels, diabetes, and about 3% of type 1 diabetes patients initially present
increasing the risk of hypoglycemia. with DKA; the incidence is two episodes per 100 patient-years of
Similarly, fluid therapy can lead to fluid overload and other diabetes. Patients with type 2 diabetes can also develop it, though
complications, particularly in patients with underlying this is less typical[6,7]. Although the incidence of diabetic ketoa-
comorbidities[2]. To adequately address these challenges, there is cidosis in developing nations is unknown, it may be greater than
a need for a comprehensive review of immediate care for severe in developed countries[8]. Whites have a greater prevalence of type
diabetic ketoacidosis[4]. Such a review would synthesize current 1 diabetes, contributing to the higher incidence of DKA in this
research findings, provide evidence-based recommendations, and racial group. For unknown causes, females are slightly more likely
highlight areas where further research is needed. than males to develop DKA. Young ladies with type 1 diabetes
frequently experience recurrent DKA, which is primarily brought
Objectives on by failing to administer insulin therapy[6,9]. DKA is much more
frequent in young children and teenagers than in adults among
This review aims to comprehensively analyze the current state of
people with type 1 diabetes; however, patients with diabetes may
immediate care for severe diabetic ketoacidosis. It will cover the
experience DKA at any age. Intervention is feasible between the
pathophysiology, clinical manifestations, and management of
onset of symptoms and the development of DKA, although
diabetic ketoacidosis, focusing on evidence-based interventions.
numerous factors (such as ethnic minority, lack of health insur-
Furthermore, the study will highlight the challenges associated
ance, lower BMI, preceding infection, delayed treatment, etc.)
with immediate care for severe diabetic ketoacidosis and provide
influence the risk of DKA among children and young people[9].
recommendations for addressing these challenges. It will be an
essential resource for healthcare professionals managing severe
Pathophysiology
diabetic ketoacidosis. This review can improve patient outcomes
and reduce the morbidity and mortality associated with severe The abnormal physiology seen in a diabetic patient with ketoaci-
diabetic ketoacidosis by providing evidence-based guidance. dosis is due to absolute or relative insulin deficiency with the rise in
hormones that put the body in a catabolic state and cause insulin
resistance leading to hyperglycemia, hyperketonemia, hyper-
Review osmolarity, and electrolyte imbalances. These hormones include;
Methodology glucagon, growth hormone, and catecholamines (epinephrine and
norepinephrine)[10]. The event that most commonly precipitates
This comprehensive review compiles and evaluates recurrent and diabetic ketoacidosis is usually a loss of insulin activity or increased
dominant topics discussed in the literature regarding the epide- demand for insulin, which can occur due to missed insulin doses,
miology, pathophysiology, and emergent therapy for patients improper administration of insulin, or the presence of infections in
with diabetic ketoacidosis, a complication of type 1 diabetes a diabetic patient[11]. It can lead to an inability to transport glucose
(T1DM) and less frequently type 2 diabetes (T2DM). To attain intracellularly; when this occurs, most cells cannot utilize glucose
the purpose of the study, the authors undertook an exhaustive and for energy, so intracellular hunger and starvation begin. Most cells
advanced Pubmed search. Pubmed is an electronic database that shift to free fatty acids (FFA) as an energy source[12,13]. Without
serves as a search engine and gives access to more than 35 million insulin, there becomes a plethora of FFA in the bloodstream
MEDLINE articles that can be cited (medical, biomedical, nur- because insulin impedes the lipolysis of adipocytes into glycerol
sing, life sciences, etc.). We used Boolean operators to combine the and FFA[8]. These abundantly circulating FFA are taken to the liver
search terms and phrases; epidemiology, pathophysiology, diag- and transported to its mitochondria for oxidation; then, ketone
nosis, and emergent therapy for patients with diabetic ketoaci- bodies are formed, including beta-hydroxybutyrate, acetone, and
dosis. We also entered the vital alternative terms into the search acetoacetate. Insulin checks the biochemical process, but excessive
for a broader reach. The review was limited to articles published ketone production results from insufficient insulin[14]. In uncom-
within the past decade (2012–2022) and was not restricted to a plicated diabetes or starvation, triglycerides usually predominate
specific region. We used only English language articles from ketones. The ketones produced do not overwhelm the body’s
academic journals with peer review. In addition, the study inclu- ability to get rid of them, putting it in a state of ketosis[15].
ded articles with both abstracts and full texts to facilitate Glucagon, catecholamines, cortisol, and growth hormone also
screening. Thirty-seven articles popped up after the filters were significantly increase blood glucose through gluconeogenesis and
applied. After reading through the abstracts of the initial results to glycogenolysis[15]. The release of these hormones can also be a
screen for eligibility, six papers were eventually selected since they response to stress, which can take the form of infections (i.e.,
also provided the most recent discussions regarding the topic. urinary tract infections and respiratory tract infections, especially
the lower tract); trauma; myocardial infarction; acute pancreatitis;
Definition and epidemiology burns; surgery; strokes; substance abuse; and so on[16]. These
stressors cause a release in inflammatory cytokines that increase
Diabetic ketoacidosis is a severe acute metabolic complication of
insulin counter-regulatory hormones like glucagon, catechola-
diabetes mellitus characterized by hyperglycemia, hyperketonae-
mines, cortisol, and growth hormone[17]. These hormones put the
mia, and metabolic acidosis. Patients have high insulin require-
body in a catabolic state, causing more lipolysis and proteolysis to
ments, eventually depleting their body insulin[5]. This insulin
synthesize glucose, which worsens hyperglycemia[18].
deficiency leads to an excessive breakdown of fat, resulting in an
excessive build-up of ketone bodies. Despite improvements in
Causes
diabetic patients’ self-care, DKA still accounts for 14% of all
hospital admissions of diabetic patients and 16% of all deaths The commonest precipitants of diabetic ketoacidosis are poor
linked to diabetes[4]. DKA commonly exists in people with type 1 compliance with insulin therapy, infections, and a new diagnosis

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of diabetes[19]. The most common precipitating factor of diabetic dysfunction or in those who are in patients[11]. Several drugs,
ketoacidosis in type 1 diabetes patients is nonadherence to such as glucocorticoids or thiazides, are well-known causes of
treatment, while infections are the most common precipitant in hyperglycemia that may lead to DKA. Clinicians should also
type 2 diabetes patients[20]. Other causes are vascular events (e.g., consider DKA in patients taking atypical antipsychotic drugs
acute coronary syndrome, cerebrovascular accidents, critical who present with hyperglycemia[23]. Atypical antipsychotic
limb ischemia, bowel ischemia, and shock); excessive alcohol drugs have increased the frequency of diabetes, glucose intol-
intake; illicit drugs such as cocaine and methamphetamine; erance, and DKA. The healthcare provider should measure
antipsychotic drugs, for example, clozapine, risperidone, and such patients’ anion gap and ketone levels. Another type of
olanzapine[19]. antipsychotic drug must be chosen to help resolve this
complication[24,25]. The presentation of a patient with DKA
Laboratory abnormalities and diagnosis varies substantially depending on the severity of the episode[5].
Mild or moderately ill patients may describe vague symptoms
In 2003, the American Diabetes Association modified the diag- of fatigue, lethargy, poor appetite, or headache. In type 1
nostic criteria of DKA by introducing severity categories of mild, diabetes, the history of polyuria and polydipsia may be rela-
moderate, and severe, as displayed in Table 1[2,21]. tively recent, but in type 2 diabetes, these symptoms may have
Abnormal changes in laboratory values give a significant clue been building for weeks to months[8]. Nausea, vomiting, and
of what exactly happens in patients with suspected diabetic abdominal pain are commonly seen in DKA and may be
ketoacidosis[2,21–23]. related to the combined effects of dehydration, hypokalemia,
The diagnosis of DKA consists of a triad of hyperglycemia, ketonemia, and delayed gastric emptying[24]. Signs of dehy-
ketonemia, and metabolic acidosis. dration, including poor skin turgor, decreased axillary sweat,
All patients with positive ketones, constitutional symptoms, or postural hypotension, may be present on physical
or suspicion of DKA and significantly elevated blood glucose examination[2]. Kussmaul respirations (a pattern of deep
levels [ > 13.9 mmol/l ( > 250 mg/dl)] should have electrolytes breathing and hyperventilation in response to metabolic
and blood gases checked to look for an anion gap metabolic acidosis) may be present[5]. Patients’ breath may smell fruity
acidosis[2]. Significantly in type 1 diabetes, DKA can develop due to increased acetone from ketonemia, but the absence of
within hours if you stop insulin injections or an insulin pump this finding does not rule out DKA. One examination aspect
malfunctions[21]. The new American Diabetes Associa- that can be confusing is abdominal tenderness, which may
tion definition of DKA includes a blood glucose level of resolve with the treatment of DKA or reflect a more acute
13.9 mmol/l (250 mg/dl)[2]. Many studies show that DKA is abdominal process that precipitates DKA[19]. Abdominal pain
infrequent at lower levels except in situations with poor oral correlates with the level of acidosis[15]. The physical exam-
intake or pregnancy[22]. It is also essential to consider DKA in ination should identify potential precipitating factors, such as
differential diagnoses for patients with anion gap metabolic infections or cardiovascular events. Patients may have mental
acidosis. Check serum glucose even when the patient has no status changes ranging from mild lethargy to delirium or
history of diabetes[15]. Consider DKA if the serum glucose is coma. The most severe cases have features like hypotension,
more significant than 13.9 mmol/l (250 mg/dl), but an elev- tachycardia, and coma[20]. Capillary blood ketone measure-
ated glucose level alone is insufficient to diagnose DKA. ment is a relatively new quantitative and enzymatic test that
Suspect DKA in patients with diabetes with a concurrent infe- determines levels of 3-β-hydroxybutyrate, one of the three
ction, stroke, myocardial infarction, or other serious illness[13]. ketone bodies[13]. The equipment is similar to that patients use
These intercurrent illnesses should be sought and treated for home blood glucose determination, but it requires specific
aggressively[13]. Similarly, it is vital to consider DKA when strips. However, checking capillary blood ketones is much
patients with diabetes experience nausea and vomiting, even if more expensive than checking urine ketones, and further
the blood sugar level is less than 13.9 mmol/l (250 mg/dl)[10]. clinical studies are needed to define the most appropriate role
Euglycemic DKA occurs more often in patients who have not for β-hydroxybutyrate monitoring[24]. If clinical suspicion of
eaten but continue taking insulin[12]. A blood sugar level of DKA is high, a negative urine dipstick for ketones does not
less than 13.9 mmol/l (250 mg/dl) occurs in 1–7% of reported exclude DKA. Clinicians should know that urine test sticks do
DKA cases and seems more common in patients with hepatic not measure β-hydroxybutyrate, the predominant ketone.
Acetoacetate measured on the dipstick may not be high until
Table 1
later during the illness[23]. Arterial blood gas assessment is
generally considered the most reliable method to evaluate the
Diagnostic criteria and severity of diabetic ketoacidosis
degree of acidosis in DKA, but a venous pH may be a more
Mild Moderate Severe practical alternative. The average anion gap is 7–9 mmol/l but
Plasma glucose (mmol/l) >13.9 >13.9 >13.9 is ~25 mmol/l in DKA[2]. Rarely do patients with DKA have
Arterial pH 7.25–7.30 7.00–7.24 < 7.00 mixed acidosis and alkalosis with a pH close to normal.
Serum bicarbonate (mmol/l) 15–18 10–14.9 < 10 However, this unexpected laboratory result should not affect
Urine ketones ++ ++ +++ the treatment of DKA[17]. Determination of the arterial blood
Serum ketones +++ +++ +++ gas may be optional. Most DKA guidelines indicate that
Anion gap >10 >12 >12 hyperglycemia of more than 13.9 mmol/l is necessary for
Sensorium Alert Alert/drowsy Stupor/coma
diagnosing DKA; however, this is not an absolute requirement,
Serum sodium Normal Low Low
as there are reports about DKA without hyperglycemia[20].
Serum potassium Normal High High
Serum phosphate Normal High High DKA without hyperglycemia is reported chiefly during
pregnancy and in patients with prolonged vomiting or

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starvation[9]. It can also occur in patients with liver failure or Table 3

alcohol abusers[9]. Ketone bodies are produced in the liver Endocrine society’s clinical practice guideline for hospitalized
from acetyl-CoA liberated during lipolysis from fatty acids. patients with diabetes
For DKA to develop, an absolute or relative insulin deficiency In patients with impaired glycemic control should be on continuous glucose monitoring
must be present. Three ketone bodies are produced: acetone devices as they effectively prevent hypoglycemic crises.
(resulting in the fruity odor of DKA patients), acetoac- Scheduled insulin therapy should be administered to in patients on glucocorticoid
etate, and β-hydroxybutyrate (β-OHB). β-OHB is the most therapy or direct enteral nutrition should they develop hyperglycemia.
prominent contributor to metabolic acidosis in patients with Outpatients on regular insulin pump therapy who are psychologically and physically fit
DKA[18]. Acetone does not contribute to acidosis and is not may self-manage the device with the supervision of medical personnel.
Education of admitted diabetic patients on essential management of the condition aids in
usually measured as such. Acetoacetate can be measured in the
reasonable glycemic control after discharge and decreases the chance of hospital
urine with a urine dipstick utilizing the nitroprusside
readmission.
reaction[10]. As DKA resolves, β-OHB is oxidized to acet- Diabetic patients being scheduled for elective surgery are desired to have a preoperative
oacetate. Therefore, if only a urine ketone dipstick procedure HbA1c of <8% and an immediate preoperative blood glucose of <180 mg/dl as it
is done, it might give the impression that the condition is not improves the patient’s postoperative condition.
improving. Blood ketones can be measured with a point of Carbohydrate-containing drinks should not be given to preoperative patients with
care (bedside) meter utilizing capillary finger prick blood[10]. diabetes.
This measures β-OHB directly and accurately[11,12]. The Correctional insulin can be used as the sole initial management for hospital admissions
American Diabetic Association recommends that the blood of newly recognized hyperglycemia or well-controlled diabetes.
ketone measurement of β-OHB is preferable to urine mea- In patients previously on insulin therapy with a continuous blood glucose of > 180 mg/dl
should be placed on scheduled insulin therapy.
surement for diagnosing and monitoring DKA[8]. An arterial
In some patients with type 2 diabetes with milder degrees of hyperglycemia, a Dipeptidyl
pH of less than 7.3 should be present in diagnosing DKA. The
peptidase inhibitor can be used with correction insulin, Provided there are no
measurement of pH or serum bicarbonate is essential for the contraindications to using any of them.
diagnosis and estimation of the severity of DKA[4]. The pH is
also an important measure to assess improvement and treat-
ment adjustment. A venous pH determination would probably
Treatment
be sufficient unless respiratory function must also be
evaluated[12]. The venous pH is, on average, 0.03 lower than Therapy goals in patients with hyperglycemic crises include
the arterial pH[23]. improving the circulatory volume and tissue perfusion, gradual
reduction of serum glucose and osmolality, correcting elec-
Differential diagnosis trolyte imbalance, and identifying and promptly treating co-
Diabetic ketoacidosis may have a diverse and complex pre- morbid precipitating causes. Successful treatment of DKA
sentation, which makes it share many similarities in the way and requires frequent monitoring of patients regarding the above
manner it presents compared to other common pathol- goals by clinical and laboratory parameters. Table 2 below
ogies; hence, other common pathologies may mimic diabetic illustrates the initial management of patients with diabetic
ketoacidosis[1]. It is, therefore, essential to rule out other ketoacidosis[2,26].
pathologies with similar presentations whenever a case of dia- A patient with diabetic ketoacidosis might have normal potas-
betic ketoacidosis is suspected. Differentials include; starvation sium levels before the initiation of treatment; the medical practi-
ketoacidosis, pancreatitis, alcoholic ketoacidosis, lactic acidosis, tioner should take caution to prevent severe hypokalemia after
uremia, overdose on diabetic medication, hyperosmolar hyper- initiating insulin therapy. Table 3 shows endocrine society’s clinical
glycemic nonketotic syndrome, and myocardial infarction[2]. practice guideline for hospitalized patients with diabetes[2,26–29].

Table 2
Detailed management of patients with diabetic ketoacidosis
Fluid therapy DKA is a volume-depleted state with an estimated 6 l of total body water deficit. Initial fluid therapy aims to increase intravascular volume and ensure sufficient
urine flow. We advise isotonic saline should be administered as the first beverage at 15–20 ml/kg of body weight per hour or 1–1.5 l during the first hour.
The choice of the fluid for additional replenishment depends on the degree of hydration, the level of serum electrolytes, and the output of the urine. Over
12–24 h, replacing half of the expected sodium and water deficit is appropriate. Hydrating fluid in the first hour of therapy before insulin administration
provides time to obtain serum potassium. Osmotic diuresis and the modulation of counter-regulatory hormone secretion are the mechanisms for lowering
blood sugar.
Insulin therapy Insulin administered in physiologic doses is essential for DKA treatment. Administer an IV bolus of regular insulin (0.1 U/kg body weight) followed by a
0.1 U/kg/hr constant infusion of regular insulin. The insulin rate should be reduced to 0.05 U/kg/hr when plasma glucose hits 200–250 mg/dl. The insulin
infusion rate should change to maintain blood glucose levels. Regular insulin is best administered via continuous IV infusion due to its short half-life and
simple titration.
Potassium therapy DKA patients with acidosis and insulinopenia have mild to moderate hyperkalemia due to acidosis and insulin depletion. Insulin therapy decreases serum
potassium levels. Acidosis correction, volume enlargement, and potassium replacement are commenced when serum levels drop below 5.3 mmol/l.
Bicarbonate therapy Bicarbonate therapy has neither a chance of benefit nor benefit in DKA, according to a prospective randomized study of patients with a pH between 6.9 and
7.1. Adult patients with pH 6.9 should be given 100 mmol sodium bicarbonate in 400 ml sterile water with 20 mmol KCl administered at 200 ml/h for 2 h
until the pH rises to 7.0. Treatment continues every 2 h if necessary.
Phosphate therapy Phosphate may be used in individuals experiencing adverse effects from hypophosphatemia, but may cause hypocalcemia when administered in large doses.
Nursing aspects of DKA Nursing management is essential for patients with comatose or pre-comatose states, and regular maintenance of infusions, nasogastric tubes, CVP lines,
urine catheters, ECG monitors, etc. Monitor temperature, pulse, blood pressure, respiration, and cognitive state every hour to confirm progress.

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This guideline addresses several crucial aspects of care precise revising the text; A.O. I.: project administration, editing, concept
for inpatient management of noncritically ill patients with dia- rephrasing; P.U.N.: literature search, writing, and editing; M.O.
betes or newly recognized hyperglycemia that can potentially K.: editing, concept rephrasing, and editing; C.E.: drafting and
improve clinical outcomes in the hospital and following discharge. revising the article; A.I.B.: concept rephrasing and maintenance of
This guideline addresses and updates some of the standards of data research integrity; O.A.: preparation, typing, editing; O.S.O.:
care for glycemic management for noncritically ill-hospitalized methodology and drafting of conclusion; F.O.J.: project admin-
adult patients with diabetes[30]. istration, review, and editing; H.I.R.-Y.: editing, concept
rephrasing, and editing.
Conclusions
Conflicts of interest
Diabetic ketoacidosis is often a severe medical emergency that results
in a complication of diabetes. When the diagnosis of diabetic In compliance with the ICMJE uniform disclosure form, all
ketoacidosis is made, the blood glucose level is higher than 250 mg/dl, authors declare the following: Payment/services info: All authors
the bicarbonate level is less than 15 mmol/l, the arterial pH is less than have declared that no financial support was received from any
7.3, and there is ketonuria or ketonemia. It occurs primarily in organization for the submitted work.
patients with type 1 diabetes. The incidence is roughly two episodes
per 100 patient-years of diabetes, with about 3% of patients with
type 1 diabetes initially presenting with diabetic ketoacidosis. It can Research registration unique identifying number
occur in patients with type 2 diabetes as well; however, this is less (UIN)
common. Diabetic ketoacidosis usually occurs due to absolute or
None.
relative insulin lack accompanied by increased glucagon, cortisol,
growth hormone, and epinephrine. This insulin deficiency enhances
hepatic gluconeogenesis, glycogenolysis, and lipolysis leading to Guarantor
severe hyperglycemia, ketoacidosis, and ketonuria.
In most cases, there are precipitating factors, which could be: Chukwuka Elendu, E-mail: elenduchukwuka@yahoo.com.
underlying infection, missed insulin treatment, previously
unknown diabetes, surgical stress, etcetera. Prompt diagnosis and
treatment are essential to improve patient outcomes. Treatment Provenance and peer review
involves fluid resuscitation, insulin administration to correct Commissioned, externally peer reviewed.
hyperglycemia, correction of acidosis, electrolyte imbalances, and
treatment of underlying causes or precipitants. The prognosis of
adequately treated patients is excellent. Data availability statement
Data will be made available by the authors upon reasonable
Ethics statement request.
It was exempted and waived at my institution.
Institutional review board statement
Patient consent The study was conducted in accordance with the Declaration of
Helsinki and approved by the Ethics Board of the Mayo Clinic
Patient consent was waived due to the minimal risk nature of the
(IRB ID: 21-007698).
observational chart review study.

Sources of funding Informed consent statement

All authors have declared that they have no financial relation- Patient consent was waived due to the minimal risk nature of the
ships at present or within the previous three years with any observational chart review study.
organizations that might have an interest in the submitted work.
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