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Why Do You Get Leukocytosis In Dka?

15l. Loriaux (ed.), Endocrine Emergencies: Recognition And Treatment, Contemporary Endocrinology 74, Doi 10.1007/978-1-62703-697-9_2, © Springer Science+business Media New York 2014

15l. Loriaux (ed.), Endocrine Emergencies: Recognition And Treatment, Contemporary Endocrinology 74, Doi 10.1007/978-1-62703-697-9_2, © Springer Science+business Media New York 2014

Précis 1. Clinical setting—Any altered state of well being in the context of signifi cant hyperglycemia in a patient with type 1 (DKA) or advanced type 2 diabetes mel- litus (DKA or HHS), particularly during acute illness, may signify one of these diabetic emergencies. 2. Diagnosis (a) History: Most patients with diabetic ketoacidosis (DKA) or with hyperos- molar hyperglycemic state (HHS) will have a history of diabetes, and a his- tory of altered insulin dose, infection, signifi cant medical “stressâ€. Antecedent symptoms of polyuria and polydipsia, lassitude, blurred vision, and mental status changes may predominate the clinical picture. With DKA, abdominal pain and tachypnea are often present. (b) Physical examination usually reveals an altered sensorium, signs of volume contraction/dehydration (tachycardia, hypotension, dry mucus membranes, “tenting†of the skin); in DKA, the odor of acetone in the breath. (c) Laboratory evaluation. The diagnostic criteria for DKA include blood glu- cose above 250 mg/dL, arterial pH < 7.30, serum bicarbonate < 15 mEq/l Chapter 2 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome Beatrice C. Lupsa and Silvio E. Inzucchi B. C. Lupsa , M.D. (*) • S. E. Inzucchi , M.D. Section of Endocrinology , Yale University School of Medicine , Yale-New Haven Hospital, 333 Cedar Street, FMP 107 , P.O. Box 208020 , New Haven , CT 06520 , USA e-mail: [email protected] 16 and moderate degree of ketonemia and/or ketonuria. Patients with HHS present with extreme hyperglycemia (blood glucose > 600 mg/dL), increased osmolality (> 320 mOsm/kg) and profound dehydration/volume contrac- tion. The laboratory evaluation of a patient with hyperglycemic emergency should include measurement of blood glucose and he 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 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 >>

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 >>

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci Continue reading >>

Thyroid Storm Presenting As Psychosis: Masked By Diabetic Ketoacidosis

Thyroid Storm Presenting As Psychosis: Masked By Diabetic Ketoacidosis

While extremely uncommon, diabetic ketoacidosis (DKA) and thyroid storm (TS) are endocrine emergencies that can coexist. We describe a case with a confounding clinical presentation that identifies these two emergencies within the setting of sepsis and influenza. Case A 69-year-old diabetic female was found by the paramedic staff to be disoriented. She demonstrated tachycardia and had a foul-smelling abdominal wound. Laboratory evaluation revealed DKA, leukocytosis, influenza B, and urinary tract infection. After appropriate management in the intensive care unit, the DKA resolved the following morning. However, the patient developed a fever, and her psychosis became more pronounced. Extensive analysis was performed but did not explain her mental status. The patient was found to have thyroid stimulating hormone of 0.06 mIU/mL, free T4 (thyroxine) of 2.38 ng/dL, and total T3 (triiodothyronine) of 72 ng/dL. Based on the Burch and Wartofsky criteria (score of 65), TS was diagnosed. Based on more recent diagnostic criteria suggested by Akamizu et al., the patient met criteria for TS grade 1. Within several hours of initiating treatment, the patient's mental state and tachycardia improved, and her psychosis resolved by the third day. This case highlights the importance of recognizing the clinical diagnosis of TS, as the magnitude of thyroid hormone derangements may not correlate with clinical severity. While rare, DKA and TS can simultaneously occur and are associated with increased morbidity and mortality if not promptly recognized and treated. 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 >>

Infection As A Trigger Of Diabetic Ketoacidosis In Intensive Care—unit Patients

Infection As A Trigger Of Diabetic Ketoacidosis In Intensive Care—unit Patients

Together with hyperglycemic coma, diabetic ketoacidosis (DKA) is the most severe acute metabolic complication of diabetes mellitus [ 1 ]. Defined by the triad hyperglycemia, acidosis, and ketonuria, DKA can be inaugural or complicate known diabetes [ 2 ]. Although DKA is evidence of poor metabolic control and usually indicates an absolute or relative imbalance between the patient's requirements and the treatment, DKA-related mortality is low among patients who receive standardized treatment, which includes administration of insulin, correction of hydroelectrolytic disorders, and management of the triggering factor (which is often cessation of insulin therapy, an infection, or a myocardial infarction) [ 3–8 ]. Although there is no proof that diabetics are more susceptible to infection, they seem to have more difficulty handling infection once it occurs [ 9 , 10 ]. Indeed, several aspects of immunity are altered in diabetic patients: polymorphonuclear leukocyte function is depressed, particularly when acidosis is present, and leukocyte adherence, chemotaxis, phagocytosis, and bactericidal activity may also be impaired [ 11–15 ]. Joshi et al. [ 10 ] reported recently on the lack of clinical evidence that diabetics are more susceptible to infection than nondiabetic patients. Nevertheless, infection is a well-recognized trigger of DKA. Earlier studies have investigated the prevalence of infection as a trigger of DKA and the impact of antimicrobial treatment [ 2 , 15–18 ]. However, none of these studies were of intensive care unit (ICU) patients only. Furthermore, most were descriptive, included small numbers of patients, used univariate analysis only, and did not designate infection as the sole outcome variable of interest. Efforts to identify correlates of infection h 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 >>

Pseudohyponatremia Definition And Causes

Pseudohyponatremia Definition And Causes

Pseudohyponatremia is not true hyponatremia but a false result of the measurement of blood sodium levels usually caused by 1: Hyperlipidemia (hypertriglyceridemia, hypercholesterolemia 7) Hyperproteinemia (for example, in multiple myeloma 8 or intravenous infusion of immunoglobulins) Radiocontrast used in chronic renal insufficient patients. Pseudohyponatremia is not a medical condition, has no symptoms and requires no treatment. Explanation: True hyponatremia means the decrease of sodium levels in the aqueous phase of the blood serum. Pseudohyponatremia is a false result of certain older tests (flame-emission spectrophotometry and indirect potentiometry I-ISE) that measure sodium levels in the whole serum (aqueous and nonaqueous phase). When the volume of the nonaqueous phase of the serum increases due to severely increased lipid or protein levels or radiocontrast substances or dextran, these tests show hyponatremia, but this is only pseudohyponatremia, because the sodium levels in the aqueous phase of the serum remain unchanged 1,3. Newer tests that use direct potentiometry with ion-specific Na+ electrodes (D-ISE), which measure sodium only in the aqueous part of the serum are not affected by hyperlipidemia or hyperproteinemia 1,3. Correction Formula for Pseudohyponatremia in Hypertriglyceridemia and Hyperlipidemia Plasma triglycerides (g/L) x 0.002 = mEq/L decrease in Na+ Plasma proteins – 8 (g/L) x 0.025 = mEq/L decrease in Na+ Reference: 2 Other Typical Changes Associated With Pseudohyponatremia Increased blood lipids or proteins result not only in pseudohyponatremia but also in false low levels of potassium (pseudohypokalemia), uric acid and blood urea nitrogen (BUN). The proliferation of the blood cells: leukocytosis, thrombocytosis, polycythemia vera is not as Continue reading >>

Prediction And Rate Of Infections In Diabetes Mellitus Patients With Diabetes Ketoacidosis In Penang, Malaysia

Prediction And Rate Of Infections In Diabetes Mellitus Patients With Diabetes Ketoacidosis In Penang, Malaysia

Syed Wasif Gillani1*, Syed Azhar Syed Sulaiman1, Shameni Sundram2 1School of Pharmaceutical Sciences, Universiti Sains Malaysia, Pulau Pinang, Malaysia 2Hospital Pulau Pinang, Pulau Pinang, Malaysia Email: *[email protected] Keywords: Diabetes Mellitus; Diabetes Ketoacidosis; Infections; Predictors; Rate of Infection Study aimed to determine the rate and prediction of infection in diabetes mellitus patients ≥ 18 year, with diabetic ketoacidosis (DKA). Retrospective cohort study design was adopted to achieve the objectives. Universal sampling technique was employed for data collection among Diabetes ketoacidosis patients, over a period of 3 years (Jan 2008-Dec 2010). Statistical package for social sciences used to analyze data. Over a 3-year period, total of 967 admissions were identified. Of it, 112 (11.6%) with no infection, 679 (70.2%) with bacterial infection and 176 (18.2%) with presumed viral infection. The mean WBC for all the patients was 18,177 (±9431). 721 (74.6%) had leukocytosis, as defined by a WBC ≥ 15,000/mm3. WBC, differential, leukocytosis, as well as sex, temperature were not significant predictors (p > 0.05) of bacterial infection. There was significant (p < 0.05) difference of age between the 3 groups, age above 57 years have high rate of infection as compared to age below and equal 57 years. The infection rate in elderly patients with DKA was high and majority of them had lack of clinical evidence. Major bacterial infections with potential serious sequel were particularly common (33.3%), among every third patient being presumed to have serious consequences. It is commonly believed that acute infectious illness can precipitate episodes of ketoacidosis in patients with diabetes mellitus. For this reason, a diligent search for bacterial infect Continue reading >>

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 >>

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