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Dka Lab Values Co2

Abg’s—it’s All In The Family

Abg’s—it’s All In The Family

By Cyndi Cramer, BA, RN, OCN, PCRN RealNurseEd.com 3.0 Contact Hour Self Learning Module Objectives: Identify the components of the ABG and their normal ranges Interpret ABG values and determine the acid base abnormality given Identify the major causes of acid base abnormalities Describe symptoms associated with acid base abnormalities Describe interventions to correct acid base abnormalities Identify the acceptable O2 level per ABG and Pulse Oximetry Identify four causes of low PaO2 The Respiratory System (Acid); CO2 is a volatile acid If you increase your respiratory rate (hyperventilation) you "blow off" CO2 (acid) therefore decreasing your CO2 acid—giving you ALKLAOSIS If you decrease your respiratory rate (hypoventilation) you retain CO2 (acid) therefore increasing your CO2 (acid)—giving you ACIDOSIS The Renal System (Base); the kidneys rid the body of the nonvolatile acids H+ (hydrogen ions) and maintain a constant bicarb (HCO3). Bicarbonate is the body’s base You have Acidosis when you have excess H+ and decreased HCO3- causing a decrease in pH. The Kidneys try to adjust for this by excreting H+ and retaining HCO3- base. The Respiratory System will try to compensate by increasing ventilation to blow off CO2 (acid) and therefore decrease the Acidosis. You have Alkalosis when H+ decreases and you have excess (or increased) HCO3- base. The kidneys excrete HCO3- (base) and retain H+ to compensate. The respiratory system tries to compensate with hypoventilation to retain CO2 (acid) To decrease the alkalosis Compensation The respiratory system can effect a change in 15-30 minutes The renal system takes several hours to days to have an effect. RESPIRATORY ACIDOSIS: pH < 7.35 (Normal: 7.35 - 7.45) CO2 > 45 (Normal: 35 – 45) 1. Causes: Hypoventilation a. Depressio Continue reading >>

Arterial Blood Gases (blood Gases), Acidosis And Alkalosis

Arterial Blood Gases (blood Gases), Acidosis And Alkalosis

Sample The better choice is the Radial artery. The sample may be taken from the femoral artery or brachial. The tests are done immediately because oxygen and carbon dioxide are unstable. Arterial blood is better than the venous blood. For arterial blood don't use the tourniquet and no pull on the syringe plunger. For venous blood syringe or tubes are completely filled and apply a tourniquet for few seconds. Arterial VS Venous blood Arterial blood gives good mixture of blood from various areas of the body. Venous blood gives information of the local area from where the blood sample is taken. Metabolism of the extremity varies from area to area. Arterial blood measurement gives the better status of the lung oxygenating the blood. Arterial blood gives information about the ability of the lung to regulate the acid-base balance through retention or release of CO2. Precautions for the collection of blood Avoid pain and anxiety to the patient which will lead to hyperventilation. Hyperventilation due to any cause leads to decreased CO2 and increased pH. Keep blood cool during transit. Don't clench finger or fist. This will leads to lower CO2 and increased acid metabolites. pCO2 values are lower in the sitting or standing position in comparison with the supine position. Don't delay the performance of the test. Avoid air bubbles in the syringe. Excess of heparin decreases the pCO2 may be 40% less. Not proper mixing of the blood before running the test. Purpose of the test This test is done on the mostly hospitalized patient. Mostly the patients are on ventilator or unconscious. For patients in pulmonary distress. To assess the metabolic (renal) acid-base and electrolytes imbalance. Its primary use is to monitor arterial blood gases and pH of blood. Also used to monitor oxygenatio Continue reading >>

Co2 Blood Test

Co2 Blood Test

What is a CO2 blood test? A CO2 blood test measures the amount of carbon dioxide (CO2) in the blood serum, which is the liquid part of blood. A CO2 test may also be called: a carbon dioxide test a TCO2 test a total CO2 test bicarbonate test an HCO3 test a CO2 test-serum You may receive a CO2 test as a part of a metabolic panel. A metabolic panel is a group of tests that measures electrolytes and blood gases. The body contains two major forms of CO2: HCO3 (bicarbonate, the main form of CO2 in the body) PCO2 (carbon dioxide) Your doctor can use this test to determine if there’s an imbalance between the oxygen and carbon dioxide in your blood or a pH imbalance in your blood. These imbalances can be signs of a kidney, respiratory, or metabolic disorder. Blood gas test » Your doctor will order a CO2 blood test based on your symptoms. Signs of an imbalance of oxygen and carbon dioxide or a pH imbalance include: shortness of breath other breathing difficulties nausea vomiting These symptoms may point to lung dysfunction involving the exchange between oxygen and carbon dioxide. You will need to have your blood’s oxygen and carbon dioxide levels measured frequently if you’re on oxygen therapy or having certain surgeries. Blood samples for a CO2 blood test may be taken from either a vein or an artery. Venipuncture blood sample Venipuncture is the term used to describe a basic blood sample taken from a vein. Your doctor will order a simple venipuncture blood sample if they only want to measure HCO3. To get a venipuncture blood sample, a healthcare provider: cleans the site (often the inside of the elbow) with a germ-killing antiseptic wraps an elastic band around your upper arm to cause the vein to swell with blood gently inserts a needle into the vein and collect blood in Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>

Blood Ketones

Blood Ketones

On This Site Tests: Urine Ketones (see Urinalysis - The Chemical Exam); Blood Gases; Glucose Tests Elsewhere On The Web Ask a Laboratory Scientist Your questions will be answered by a laboratory scientist as part of a voluntary service provided by one of our partners, the American Society for Clinical Laboratory Science (ASCLS). Click on the Contact a Scientist button below to be re-directed to the ASCLS site to complete a request form. If your question relates to this web site and not to a specific lab test, please submit it via our Contact Us page instead. Thank you. Continue reading >>

End-tidal Capnography Can Be Useful For Detecting Diabetic Ketoacidosis, Monitoring Copd

End-tidal Capnography Can Be Useful For Detecting Diabetic Ketoacidosis, Monitoring Copd

End-Tidal Capnography Can be Useful for Detecting Diabetic Ketoacidosis, Monitoring COPD by Katrina DAmore, DO, MPH, Justin McNamee, DO, and Terrance McGovern, DO, MPH End-tidal capnography has gained momentum over the years as a standard for monitoring patients undergoing procedural sedation in the emergency department, with a level B recommendation coming out of ACEPs clinical policy regarding procedural sedation in 2014.1 It can identify hypoventilation earlier than other monitoring tools we have at our disposal in the emergency department, but its utility doesnt end there. It can quickly and efficiently answer clinical questions beyond that of sufficient ventilation. Are the chest compressions being performed on your cardiac arrest inadequate? Should you stop resuscitation efforts? Is your hyperglycemic diabetic in diabetic ketoacidosis (DKA)? Is that nasogastric tube in the stomach? End-tidal capnography can lend insight to these questions that emergency physicians encounter on a daily basis. End-tidal carbon dioxide (EtCO2) sensibly correlates with the pathophysiology of those and many other disease processes and can help guide decision making on your next shift. Capnography offers an indirect method to detect metabolic acidosis. EtCO2 measurements have been shown to closely estimate arterial partial pressure of carbon dioxide (pCO2) in healthy patients and also in the presence of metabolic derangements such as acidosis. The end-tidal capnogram is separated into four separate phases (see Figure 1). Phase 0 begins during the inhalation phase of the respiratory cycle and the capnogram drops precipitously from its peak level at the end of expiration. Once the patient begins to exhale (phase I), the initial expired air is predominantly dead space with little expired Continue reading >>

Lab Test

Lab Test

Measurement of serum chloride concentrations for the assessment of certain disorders manifesting with electrolyte abnormalities. This test is performed as part of multiphasic testing for what is usually called "electrolytes." By itself, this test does not provide much information, but with interpretation of the other electrolytes, chloride can given an indication of acid-base balance and hydration status. Neonates, Cord Blood: 96-104 mEq/L (96-104 mmol/L) Neonates, 0 to 30 days: 98-113 mEq/L (98-113 mmol/L) Children, older than 30 days: 98-107 mEq/L (98-107 mmol/L) *(PDR) Adult/elderly: 98-106 mEq/L or 98-106 mmol/L Child: 90-110 mEq/L Newborn: 96-106 mEq/L Premature infant: 95-110 mEq/L Critical Values: < 80 or > 115 mEq/L Hypokalemia - high serum chloride levels with hypokalemia are usually associated with low serum bicarbonate levels and may reflect either metabolic acidosis (e.g., diarrhea renal tubular acidosis) or respiratory alkalosis (e.g., cirrhosis, sepsis salicylate poisoning). Low serum chloride levels with hypokalemia are usually associated with increased serum bicarbonate and metabolic alkalosis, suggesting diuretic use, vomiting, hyperaldosteronism, or abuse of licorice or laxatives as the etiology of hypokalemia. Initial evaluation and monitoring of diabetic ketoacidosis (DKA)- chloride measurement is used to calculate plasma anion gap. Hyperchloremic normal anion gap metabolic acidosis is present on admission in about 10% of patients with DKA and is present in nearly al patients after resolution of Ketonemia. During treatment, severity of hyperchloremia can be exacerbated by excessive administration of 0.9% sodium chloride for hydration. Metabolic acidosis - an elevated serum chloride level occurs in Hyperchloremic acidosis, a metabolic acidosis in whic Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Anion Gap In Diabetes Ketoacidosis

Anion Gap In Diabetes Ketoacidosis

When I left the Cardiac-Surgical ICU to go to a Medical Cardiac ICU at a Level I Trauma center, it was a big change for me. It was a whole new regime of policies, protocols, and procedures. And, it was a big chance for growth for me as a nurse. I remember one of the first patients I had when I got to the new unit. I was caring for a DKA patient and the doctors continually asking me has her gap closed? I thought to myself, What the heck are they talking about? Diabetic ketoacidosis is an EMERGENCY! It must be treated as quickly as possible to prevent coma and/or death. The patients insulin needs are unable to match their insulin supply. The body metabolizes glucose for energy, so it begins to metabolize fats and acids, which in turn, create ketones. The ketones create keto acids, which create a state of acidosis. Watch this video for an in-depth conversation about DKA: Irregular pattern of deep & rapid breathing. Patients are trying to blow off CO2 to lower acid levels DKA can often be the first manifestation of Type 1 diabetes. Chronic hyperglycemia causes damage to tissues & organs over time. The body can (for the most part) tolerate and compensate while the person is young. Additionally, younger people and children burn more calories (thus, lowering their glucose levels) than adults due to: What converts the person from a state of tolerance to a state of DKA, is an injury. Injuries are not just a physical injury like a cut or something, but any type of injury which causes the body to develop a stress response to repair itself, like infection. An Anion Gap is the difference between the measured cations and anions in the serum. There are some formulas where potassium is not added to the sodium. The rational behind that is potassium is usually a small number and may not Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

4 Evaluation 5 Management Defining features include hyperglycemia (glucose > 250mg/dl), acidosis (pH < 7.3), and ketonemia/ketonuria Leads to osmotic diuresis and depletion of electrolytes including sodium, magnesium, calcium and phosphorous. Further dehydration impairs glomerular filtration rate (GFR) and contributes to acute renal failure Due to lipolysis / accumulation of of ketoacids (represented by increased anion gap) Compensatory respiratory alkalosis (i.e. tachypnea and hyperpnea - Kussmaul breathing) Breakdown of adipose creates first acetoacetate leading to conversion to beta-hydroxybutyrate Causes activation of RAAS in addition to the osmotic diuresis Cation loss (in exchange for chloride) worsens metabolic acidosis May be the initial presenting of an unrecognized T1DM patient Presenting signs/symptoms include altered mental status, tachypnea, abdominal pain, hypotension, decreased urine output. Perform a thorough neurologic exam (cerebral edema increases mortality significantly, especially in children) Assess for possible inciting cause (especially for ongoing infection; see Differential Diagnosis section) Ill appearance. Acetone breath. Drowsiness with decreased reflexes Tachypnea (Kussmaul's breathing) Signs of dehydration with dry mouth and dry mucosa. Perform a thorough neurologic exam as cerebral edema increases mortality significantly, especially in children There may be signs from underlying cause (eg pneumonia) Differential Diagnosis Insulin or oral hypoglycemic medication non-compliance Infection Intra-abdominal infections Steroid use Drug abuse Pregnancy Diabetic ketoacidosis (DKA) Diagnosis is made based on the presence of acidosis and ketonemia in the setting of diabetes. Bicarb may be normal due to compensatory and contraction alcoholosis so the Continue reading >>

Original Article Correlation Between Peripheral Venous And Arterial Blood Gas Measurements In Patients Admitted To The Intensive Care Unit: A Single-center Study

Original Article Correlation Between Peripheral Venous And Arterial Blood Gas Measurements In Patients Admitted To The Intensive Care Unit: A Single-center Study

Introduction The acid–base and respiratory status of critical patients are commonly ascertained by means of arterial blood gas (ABG) analysis. Nevertheless, the test can cause patients to experience discomfort, and its associated complications include arterial injury, thrombosis or embolization, hematoma, aneurysm formation, and reflex sympathetic dystrophy [1,2]. A further drawback for health care providers is the possibility of a needle stick injury when performing an ABG. A comparatively safer procedure is venous blood gas (VBG) analysis, which poses fewer risks to both the patients and health care professionals. VBG may eventually take the place of ABG analysis in determining acid–base status. In contrast to earlier studies, which questioned the precision of VBG values [3–5], more recent evidences indicate a concurrence of ABG and VBG values [6–14]. However, as far as we can determine, the correlation between all parameters typically used in arterial and peripheral VBG samples as found in a broad population of intensive care unit (ICU) patients has not been studied previously. An earlier study investigated whether the similarities between ABG and VBG values are sufficient for the respiratory and dynamic acid–base conditions. For this evaluation, each patient provided multiple paired ABG and VBG samples during the length of their ICU treatment. The purpose of this study was to investigate the correlation of ABG and peripheral VBG samples for all common parameters (bicarbonate, total CO2, pH, and PCO2) in an ICU patient population exhibiting a variety of pathologies. Specific attention was given to the analysis of each patient's multiple paired arterial and venous samples. Methods A single-center, prospective trial was performed from April 2010 to September Continue reading >>

Diabetic Ketoacidosis Workup

Diabetic Ketoacidosis Workup

Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L. [17] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management. It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Base Excess

Base Excess

In physiology, base excess and base deficit refer to an excess or deficit, respectively, in the amount of base present in the blood. The value is usually reported as a concentration in units of mEq/L, with positive numbers indicating an excess of base and negative a deficit. A typical reference range for base excess is −2 to +2 mEq/L.[1] Comparison of the base excess with the reference range assists in determining whether an acid/base disturbance is caused by a respiratory, metabolic, or mixed metabolic/respiratory problem. While carbon dioxide defines the respiratory component of acid-base balance, base excess defines the metabolic component. Accordingly, measurement of base excess is defined, under a standardized pressure of carbon dioxide, by titrating back to a standardized blood pH of 7.40. The predominant base contributing to base excess is bicarbonate. Thus, a deviation of serum bicarbonate from the reference range is ordinarily mirrored by a deviation in base excess. However, base excess is a more comprehensive measurement, encompassing all metabolic contributions. Definition[edit] Pathophysiology sample values BMP/ELECTROLYTES: Na+ = 140 Cl− = 100 BUN = 20 / Glu = 150 K+ = 4 CO2 = 22 PCr = 1.0 \ ARTERIAL BLOOD GAS: HCO3− = 24 paCO2 = 40 paO2 = 95 pH = 7.40 ALVEOLAR GAS: pACO2 = 36 pAO2 = 105 A-a g = 10 OTHER: Ca = 9.5 Mg2+ = 2.0 PO4 = 1 CK = 55 BE = −0.36 AG = 16 SERUM OSMOLARITY/RENAL: PMO = 300 PCO = 295 POG = 5 BUN:Cr = 20 URINALYSIS: UNa+ = 80 UCl− = 100 UAG = 5 FENa = 0.95 UK+ = 25 USG = 1.01 UCr = 60 UO = 800 PROTEIN/GI/LIVER FUNCTION TESTS: LDH = 100 TP = 7.6 AST = 25 TBIL = 0.7 ALP = 71 Alb = 4.0 ALT = 40 BC = 0.5 AST/ALT = 0.6 BU = 0.2 AF alb = 3.0 SAAG = 1.0 SOG = 60 CSF: CSF alb = 30 CSF glu = 60 CSF/S alb = 7.5 CSF/S glu = 0.4 Base excess Continue reading >>

Diabetic Ketoacidosisworkup

Diabetic Ketoacidosisworkup

Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L. [ 17 ] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Blood tests for glucose every 1-2 h until patient is stable, then every 4-6 h Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 h Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 201 Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

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