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Why Do You Get Leukocytosis In Dka?

Original Article Acute Activation Of Peripheral Lymphocytes During Treatment Of Diabetic Ketoacidosis

Original Article Acute Activation Of Peripheral Lymphocytes During Treatment Of Diabetic Ketoacidosis

Abstract Activated peripheral T-lymphocytes are increased in both pre-insulin-dependent diabetes mellitus (IDDM) patients and in recently diagnosed IDDM patients, as well as in various forms of acute stress. We studied the in vivo T-lymphocyte activation in six patients in severe diabetic ketoacidosis (DKA) prior to treatment, after 24 h of treatment and ≥5 days after admission. Five of the six patients showed an increased percentage of activated T-lymphocytes based on the expression of HLA-DR at 24 h of treatment when compared to the admission percentage of activation (P<.05). There was no correlation to the admission serum glucose, osmolality, or electrolytes. Serum pH showed a trend toward an inverse correlation, but was not statistically significant. We speculate that T-lymphocyte activation plays a role in the progression of the acute complications of subclinical brain edema and interstitial pulmonary edema of DKA. This process could also be another factor in the progression of the chronic complications of IDDM in addition to the well-established effects of hyperglycemia and hypertension. Continue reading >>

Diabetic Emergencies-diagnosis And Clinical Management: Diabetic Ketoacidosis In Adults, Part 2

Diabetic Emergencies-diagnosis And Clinical Management: Diabetic Ketoacidosis In Adults, Part 2

Hyperglycemia Hyperglycemia in DKA is the result of reduced glucose uptake and utilization from the liver, muscle, and fat tissue and increased gluconeogenesis as well as glycogenolysis. The lack of insulin results in an increase in gluconeogenesis, primarily in the liver but also in the kidney, and increased glycogenolysis in liver and muscle.8,9 In addition, the inhibitory effect of insulin on glucagon secretion is abolished and plasma glucagon levels increase. The increase of glucagon aggravates hyperglycemia by enhancing gluconeogenesis and glycogenolysis. In parallel, the increased concentrations of the other counter-regulatory hormones enhance further gluconeogenesis. In addition to increased gluconeogenesis, in DKA there is excess production of substances which are used as a substrate for endogenous glucose production. Thus, the amino acids glutamine and alanine increase because of enhanced proteolysis and reduced protein synthesis.8,9 Hyperglycemia-induced osmotic diuresis leads to dehydration, hyperosmolality, electrolyte loss (Na+, K +, Mg 2 +, PO 4 3+, Cl−, and Ca+), and eventually decline in glomerular filtration rate. With decline in renal function, glucosuria diminishes and hyperglycemia worsens. Dehydration results in augmentation of plasma osmolality, which results in water movement out of the cells to the extracellular space. Osmotic diuresis caused by hyperglycemia results in loss of sodium in urine; in addition, the excess of glucagon aggravates hyponatremia because it inhibits reabsorption of sodium in the kidneys. With impaired insulin action and hyperosmolality, utilization of potassium by skeletal muscles is markedly decreased leading to intracellular potassium deficiency. Potassium is also lost due to osmotic diuresis. In addition, metabolic ac Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis (DKA) is a metabolic emergency occurring in Type 1 diabetes. It is characterised by the following: Acidosis: Blood pH below 7.3 or plasma bicarbonate below 18mmol/litre Ketonaemia: Blood ketones (beta-hydroxybutyrate) above 3mmol/litre Hyperglycaemia: Blood glucose levels are generally high (above 11mmol/litre), although children with known Type 1 diabetes can less commonly develop DKA with normal blood glucose levels DKA can be life threatening. The three complications which account for the majority of deaths in these children are cerebral oedema, hypokalaemia and aspiration pneumonia. An understanding of the principles discussed in the ‘Approach to the Seriously Unwell Child’ article and an awareness of the British Society of Paediatric Endocrinology and Diabetes (BSPED) guideline for DKA management (1) will help you manage these children appropriately. 31,500 children and young people under the age of 19 in the UK have diabetes. The vast majority of them (over 95%), have Type 1 Diabetes Mellitus (T1DM.) The peak age for diagnosis is between 9 and 14 years (2). In established T1DM, the risk of DKA is 1–10% per patient per year (3). Reported mortality rates from DKA in children in the UK are around 0.3%, the majority of which are attributable to cerebral oedema, which has a mortality rate of 25 % (4). T1DM can be seen as ‘starvation in the midst of plenty,’ where blood glucose levels are raised as it cannot be used for metabolism or stored due to an absolute deficiency of insulin. This leads to a rise in counter-regulatory hormones including glucagon, cortisol, catecholamines and growth hormone. The increase in these gluconeogenic hormones not only raises the blood glucose concentration further, but also leads to accelerated break down o Continue reading >>

Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness

Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness

Diabetic ketoacidosis (DKA) is an acute, life‐threatening metabolic complication of diabetes mellitus. Hyperglycaemia, ketosis (ketonaemia or ketonuria) and acidosis are the cardinal features of DKA [1]. Other features that indicate the severity of DKA include volume depletion, acidosis and concurrent electrolyte disturbances, especially abnormalities of potassium homeostasis [1,2]. We describe a type 2 diabetic patient presenting with severe generalized muscle weakness and electrocardiographic evidence of severe hyperkalaemia in association with DKA and discuss the related pathophysiology. A 65‐year‐old male was admitted because of impaired mental status. He was a known insulin‐treated diabetic on quinapril (20 mg once daily) and was taking oral ampicillin 500 mg/day because of dysuria which had started 5 days prior to admission. He was disoriented in place and time with severe generalized muscle weakness; he was apyrexial (temperature 36.4°C), tachycardic (120 beats/min) and tachypneic (25 respirations/min) with cold extremities (supine blood pressure was 100/60 mmHg). An electrocardiogram (ECG) showed absent P waves, widening of QRS (‘sine wave’ in leads I, II, V5 and V6), depression of ST segments and tall peaked symmetrical T waves in leads V3–V6 (Figure 1). Blood glucose was 485 mg/dl, plasma creatinine 5.1 mg/dl (reference range (r.r.) 0.6–1.2 mg/dl, measured by the Jaffe method), urea 270 mg/dl (r.r. 11–54 mg/dl), albumin 4.2 g/dl (r.r. 3.4–4.7 g/dl), sodium 136 mmol/l (r.r. 135–145 mmol/l), chloride 102 mmol/l (r.r. 98–107 mmol/l), potassium 8.3 mmol/l (r.r. 3.5–5.4 mmol/l), phosphorus 1.6 mmol/l (r.r. 0.8–1.45 mmol/l) and magnesium 0.62 mmol/l (r.r. 0.75–1.25 mmol/l). A complete blood count revealed leukocytosis (12 090/µl with Continue reading >>

Tropical Journal Of Pharmaceutical Research October 2012; 11 (5): 815-821 © Pharmacotherapy Group,

Tropical Journal Of Pharmaceutical Research October 2012; 11 (5): 815-821 © Pharmacotherapy Group,

Ezzeldi & Nahhas Trop J Pharm Res, October2012;11 (5): 815 Faculty of Pharmacy, University of Benin, Benin City, 300001 Nigeria. All rights reserved. Available online at Research Article Serological Prediction of infections in Diabetic Patients with Diabetes Ketoacidosis in Penang, Malaysia Syed Wasif Gillani1*, Syed Azhar Syed Sulaiman1, Shameni Sundram2, Yelly Oktavia Sari3,4, Mirza Baig5 and Mian Muhammad Shahid Iqbal6 1School of Pharmaceutical Sciences, Universiti Sains Malaysia, Pulau Pinang, Malaysia, 2Doctor, Hospital Pulau Pinang, 10990, Residential Street, Penang, 3Faculty of Pharmacy, Andalas University, Padang 25163, Indonesia, 4Discipline of Clinical Pharmacy, School of Pharmaceutical Sciences, Universiti Sains Malaysia, 11800 Penang, 5Department of Clinical Pharmacy, Aimst University, Kedah, 6School of Pharmacy and Health Sciences, International Medical University, Malaysia. Abstract Purpose: To determine the prevalence and predictors of infection in diabetic patients with diabetic ketoacidosis (DKA) who were ≥18 years. Methods: A retrospective cohort design was adopted for this study. A total of 967 diabetes ketoacidosis patients from Hospital Pulau Pinang for the 3-year period, Jan 2008 - Dec 2010, were identified and enrolled. The data were analysed, as appropriate, by Student t-test and ANOVA for the normally distributed data, Mann-Whitney U rank sum and Kruskall-Wallis tests for continuous, non-nominal data and Chi-square for dichotomous variables. Odd Ratios with 95% confidence interval (CI) were also presented where applicable. Results: Of the total diabetes ketoacidosis patients, 112 (11.6 %) were cases without infection, 679 (70.2 %) bacterial infection cases and 176 (18.2 %) presumed viral infection cases. The mean white blood count (WBC) fo Continue reading >>

Hyperglycemic Crises In Adult Patients With Diabetes

Hyperglycemic Crises In Adult Patients With Diabetes

Go to: PATHOGENESIS The events leading to hyperglycemia and ketoacidosis are depicted in Fig. 1 (13). In DKA, reduced effective insulin concentrations and increased concentrations of counterregulatory hormones (catecholamines, cortisol, glucagon, and growth hormone) lead to hyperglycemia and ketosis. Hyperglycemia develops as a result of three processes: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues (12–17). This is magnified by transient insulin resistance due to the hormone imbalance itself as well as the elevated free fatty acid concentrations (4,18). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation in the liver to ketone bodies (β-hydroxybutyrate and acetoacetate) (19), with resulting ketonemia and metabolic acidosis. Increasing evidence indicates that the hyperglycemia in patients with hyperglycemic crises is associated with a severe inflammatory state characterized by an elevation of proinflammatory cytokines (tumor necrosis factor-α and interleukin-β, -6, and -8), C-reactive protein, reactive oxygen species, and lipid peroxidation, as well as cardiovascular risk factors, plasminogen activator inhibitor-1 and free fatty acids in the absence of obvious infection or cardiovascular pathology (20). All of these parameters return to near-normal values with insulin therapy and hydration within 24 h. The procoagulant and inflammatory states may be due to nonspecific phenomena of stress and may partially explain the association of hyperglycemic crises with a hypercoagulable state (21). The pathogenesis of HHS is not as wel Continue reading >>

Diabetic Ketoacidosis Causes, Symptoms, Treatment, And Complications

Diabetic Ketoacidosis Causes, Symptoms, Treatment, And Complications

Diabetic ketoacidosis definition and facts Diabetic ketoacidosis is a life-threatening complication of type 1 diabetes (though rare, it can occur in people with type 2 diabetes) that occurs when the body produces high levels of ketones due to lack of insulin. Diabetic ketoacidosis occurs when the body cannot produce enough insulin. The signs and symptoms of diabetic ketoacidosis include Risk factors for diabetic ketoacidosis are type 1 diabetes, and missing insulin doses frequently, or being exposed to a stressor requiring higher insulin doses (infection, etc). Diabetic ketoacidosis is diagnosed by an elevated blood sugar (glucose) level, elevated blood ketones and acidity of the blood (acidosis). The treatment for diabetic ketoacidosis is insulin, fluids and electrolyte therapy. Diabetic ketoacidosis can be prevented by taking insulin as prescribed and monitoring glucose and ketone levels. The prognosis for a person with diabetic ketoacidosis depends on the severity of the disease and the other underlying medical conditions. Diabetic ketoacidosis (DKA) is a severe and life-threatening complication of diabetes. Diabetic ketoacidosis occurs when the cells in our body do not receive the sugar (glucose) they need for energy. This happens while there is plenty of glucose in the bloodstream, but not enough insulin to help convert glucose for use in the cells. The body recognizes this and starts breaking down muscle and fat for energy. This breakdown produces ketones (also called fatty acids), which cause an imbalance in our electrolyte system leading to the ketoacidosis (a metabolic acidosis). The sugar that cannot be used because of the lack of insulin stays in the bloodstream (rather than going into the cell and provide energy). The kidneys filter some of the glucose (suga Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Complication of type I diabetes result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis undiagnosed DM Presentation Symptoms abdominal pain vomiting Physical exam Kussmaul respiration increased tidal volume and rate as a result of metabolic acidosis fruity, acetone odor severe hypovolemia coma Evaluation Serology blood glucose levels > 250 mg/dL due to ↑ gluconeogenesis and glycogenolysis arterial pH < 7.3 ↑ anion gap due to ketoacidosis, lactic acidosis ↓ HCO3- consumed in an attempt to buffer the increased acid hyponatremia dilutional hyponatremia glucose acts as an osmotic agent and draws water from ICF to ECF hyperkalemia acidosis results in ICF/ECF exchange of H+ for K+ moderate ketonuria and ketonemia due to ↑ lipolysis β-hydroxybutyrate > acetoacetate β-hydroxybutyrate not detected with normal ketone body tests hypertriglyceridemia due to ↓ in capillary lipoprotein lipase activity activated by insulin leukocytosis due to stress-induced cortisol release H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted Treatment Fluids Insulin with glucose must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ be Continue reading >>

When There Are Acute Changes In Mental Status In Patients With Diabetes

When There Are Acute Changes In Mental Status In Patients With Diabetes

Author(s): Adam Lang, BS, and Kathleen Satterfield, DPM, FACFAOM As podiatric physicians in 2010, we are better trained than ever to manage patients’ problems. Even more importantly, we are well versed in making appropriate, well-timed referrals when needed. In the following case study, that particular acumen was critically important. A 78-year-old male with type 2 diabetes underwent resection of the first metatarsophalangeal base and debridement of an underlying ulcer, which has at times been infected. The plan was to inspect the bone for osteomyelitis, place the patient on oral antibiotics and not primarily close the plantar lesion, but pack it open instead. Resection of the phalangeal base would ease the deforming hallux interphalangeus. Examination revealed a hallux limitus and the physician determined that at the patient’s age and activity level, a Keller arthroplasty would serve him well, preventing further breakdown and possible osteomyelitis. The plantar lesion did not undergo primary closure but physicians packed it instead. The hospital discharged the patient within a week after bone cultures and histology showed no evidence of osteomyelitis. He received a prescription for oral antibiotics and received instruction to keep a clinic appointment in 48 hours. However, he was a no-show for his appointment. Phone calls to his home, all of which were documented, went unanswered over a period of two weeks. About a month after his discharge from the hospital, the patient went to the emergency department of the hospital accompanied by his wife. His extremity was in the same dressing he received upon preparation for discharge although now it was soiled and loose. His wife reported that they had never filled the prescription for antibiotics because they “did not und Continue reading >>

Correlation Between Peripheral White Blood Cell Counts And Hyperglycemic Emergencies

Correlation Between Peripheral White Blood Cell Counts And Hyperglycemic Emergencies

Go to: Abstract Objective: To determine the correlation between differential leukocyte counts and hyperglycemic emergencies. Methods: Fifty patients with diabetic ketoacidosis (DKA), 50 patients with diabetic ketosis (DK), 50 non-DK diabetic patients with stable glycemic control, and 50 normal controls were enrolled. Their total and differential leukocyte counts were measured and evaluated at admission and after treatment. Results: The patients with DKA and DK had higher plasma glucose levels (20.84±6.73 mmol/L, 15.55±2.6 mmol/L, respectively) and more median leukocytes (13325/mm3 and 6595/mm3, respectively) and median neutrophils (11124 /mm3 and 4125/mm3, respectively) but fewer median eosinophils (28/mm3 and 72/mm3, respectively) compared to non-DK and control groups (all p < 0.05). Acute infection increased the elevating extent. The median leukocyte counts in DK and non-DK patients (6595/mm3 and 6008/mm3, respectively) were within the normal range. The counts of total leukocytes and neutrophils were significantly higher but eosinophils lower in severe DKA cases than in mild/moderate cases (p < 0.05). When the DKA and DK and infection resolved, total leukocytes and neutrophils fell, but eosinophils increased. The counts of total leukocytes, neutrophils, and monocytes were negatively correlated with arterial pH levels (r = -0.515, r = -0.510, r = -0.517, all p < 0.001, respectively) and positively correlated with plasma glucose levels (r = 0.722, r = 0.733, r = 0.632, all p < 0.05, respectively) in DKA patients. The arterial pH level was the most significant factor affecting total leukocytes in DKA (β = 0.467, p = 0.003). The diagnosis analysis showed that higher total leukocyte and neutrophil counts and lower eosinophil counts had a significant ability to reflect t Continue reading >>

Chapter 24: Diabetic Ketoacidosis And Hyperosmolar Coma

Chapter 24: Diabetic Ketoacidosis And Hyperosmolar Coma

Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute complications of diabetes mellitus (DM). DKA is seen primarily in individuals with type 1 DM and HHS in individuals with type 2 DM. Both disorders are associated with absolute or relative insulin deficiency, volume depletion, and altered mental status. The metabolic similarities and differences in DKA and HHS are summarized in Table 24-1. DKA results from insulin deficiency with a relative or absolute increase in glucagon and may be caused by inadequate insulin administration, infection (pneumonia, urinary tract infection, gastroenteritis, sepsis), infarction (cerebral, coronary, mesenteric, peripheral), surgery, trauma, drugs (cocaine), or pregnancy. A common precipitating scenario is the pt with type 1 DM who erroneously stops administering insulin because of anorexia/lack of food intake caused by a minor illness, followed by lipolysis and progressive ketosis leading to DKA. The initial symptoms of DKA include anorexia, nausea, vomiting, polyuria, and thirst. Abdominal pain, altered mental function, or frank coma may ensue. Classic signs of DKA include Kussmaul respirations and an acetone odor on the pt's breath. Volume depletion can lead to dry mucous membranes, tachycardia, and hypotension. Fever and abdominal tenderness may also be present. Laboratory evaluation reveals hyperglycemia, ketosis (β-hydroxybutyrate > acetoacetate), and metabolic acidosis (arterial pH 6.8–7.3) with an increased anion gap (Table 24-1). The fluid deficit is often 3–5 L and can be greater. Despite a total-body potassium deficit, the serum potassium at presentation may be normal or mildly high as a result of acidosis. Similarly, phosphate may be normal at presentation despite total body phosphate depletion Continue reading >>

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Copyright © 2014 Nupur Sinha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as “accelerated starvation.” Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids. 1. Introduction A relative insulin deficient state has been well described in pregnancy. This is due to placentally derived hormones including glucagon, cortisol, and human placental lactogen which are increased in periods of stress [1]. The insulin resistance increases with gestational age Continue reading >>

Childhood Ketoacidosis

Childhood Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Diabetic ketoacidosis (DKA) is the leading cause of mortality in childhood diabetes.[1]The primary cause of DKA is absolute or relative insulin deficiency: Absolute - eg, previously undiagnosed type 1 diabetes mellitus or a patient with known type 1 diabetes who does not take their insulin. Relative - stress causes a rise in counter-regulatory hormones with relative insulin deficiency. DKA can be fatal The usual causes of death are: Cerebral oedema - associated with 25% mortality (see 'Cerebral odedema', below). Hypokalaemia - which is preventable with good monitoring. Aspiration pneumonia - thus, use of a nasogastric tube in the semi-conscious or unconscious is advised. Deficiency of insulin. Rise in counter-regulatory hormones, including glucagon, cortisol, growth hormone, and catecholamines. Thus, inappropriate gluconeogenesis and liver glycogenolysis occur compounding the hyperglycaemia, which causes hyperosmolarity and ensuing polyuria, dehydration and loss of electrolytes. Accelerated catabolism from lipolysis of adipose tissue leads to increased free fatty acid circulation, which on hepatic oxidation produces the ketone bodies (acetoacetic acid and beta-hydroxybutyric acid) that cause the metabolic acidosis. A vicious circle is usually set up as vomiting usually occurs compounding the stress and dehydration; the cycle can only be broken by providing insulin and fluids; otherwise, severe acidosis occurs and can be fatal. Biochemical criteria The biochemical criteria required for a diagnosis of DKA to be made are Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a life-threatening condition when the body has practically no insulin. This insulin deficiency results in extremely high blood sugar levels. Consequently, the muscle, fat and liver cells cannot use glucose for fuel. These cells are converted into glucose by hormones such as glucagon and adrenalin and turned into ketones through oxidation. As a result, the body uses fat for fuel. The increased levels of blood sugar are not flushed through urination. DKA is usually noticed in patients suffering from Insulin-dependent diabetes. A person can suffer from diabetic ketoacidosis if there has been severe dehydration and consequently the blood chemistry has been affected. There is accumulation of organic acids and ketones in the blood. Elevated ketone levels in the body upset its blood pH and make the blood acidic thereby triggering a toxic condition for the body's cells. Diabetic ketoacidosis is noticed when hyperglycemia exceeds 300 mg/dL. If diabetes ketoacidosis is not addressed in time, it can lead to coma and death. Surgery, infection, trauma, stroke or heart attack can also trigger diabetes ketoacidosis. Insufficient fluid intake, pancreatitis and alcohol abuse can trigger diabetes ketoacidosis. Symptoms of diabetes ketoacidosis include excessive thirst and general weakness. There is frequent urination, loss of appetite and vomiting. Other symptoms of diabetes ketoacidosis are weight loss and abdominal pain. A person suffering from DKA tends to experience low blood pressure and increased heart rate. High ketone levels can give rise to a fruity-scent on the breath and vomiting. The patient will be restless and agitated. The skin will be hot and dry and appear flushed. Patients suffering from diabetes must check their blood glucose levels if th Continue reading >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

Management Of Diabetic Ketoacidosis In Children And Adolescents

Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>

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