Back To Basics
The Case A 48-year-old woman with insulin-dependent diabetes mellitus presents to the emergency department with right upper quadrant pain, fever, and leukocytosis, prompting admission for presumed cholangitis. Overnight, the patient was made NPO (nothing by mouth) in anticipation of an endoscopic retrograde cholangiopancreatography (ERCP) the following morning. The admitting medical team ordered an insulin sliding scale for the patient, and her blood glucose levels became very difficult to control in the ensuing hours. In the morning, the patient developed an anion gap and evidence of mild diabetic ketoacidosis. The physician evaluating the patient in the morning realized that no basal insulin was ordered and instituted a more appropriate regimen of insulin, and the patient underwent an uneventful ERCP and hospitalization. This case is about a near miss, a tragic outcome narrowly averted by an alert physician who promptly corrected a series of earlier misjudgments that led to an inappropriate plan for insulin administration. The errant plan resulted in the development of diabetic ketoacidosis (DKA) in a seriously ill, infected patient who was NPO and awaiting an ERCP. If not recognized or anticipated, DKA carries the potential for lethal consequences.(1,2) A key error by the admitting team was not providing for a greatly increased basal insulin requirement, opting instead for a less effective insulin sliding scale algorithm. This decision making represented the wrong approach in this setting, an example of a rule-based error. Reason characterizes such situations as "strong but wrong" rule-based errors—the rule is strong in general but was inappropriate or misapplied in this situation.(3) Metabolic stressors such as myocardial ischemia, surgery, cardiovascular collapse Continue reading >>
An 18-year-old Patient With Type 1 Diabetes Undergoing Surgery
Description of Case An 18-year-old Caucasian male with type 1 diabetes presented to the emergency department complaining of severe left knee pain and swelling after sustaining a knee injury that occurred during a high school football match. Joint effusions were visible and palpable above the left knee, and there was significant loss of smooth motion of the knee, passively performed. Plain X rays showed no signs of fractures. The patient had had type 1 diabetes for six years, and his insulin regimen consisted of insulin glargine, 35 units at 8:00 p.m., and insulin lispro, 23 units at 8:00 a.m. and 16 units at 8:00 p.m. The patient had no apparent complications related to type 1 diabetes. On examination he was alert, his pulse was 76 bpm regular, and his blood pressure was 118/66 mm Hg. Recently, the patient had had frequent episodes of both hyperglycemia and hypoglycemia. However, he had never developed diabetic ketoacidosis (DKA). His recent HbA1c was 9.5%, demonstrating inadequate glycemic control. The patient was referred to an orthopedic surgeon, and arthroscopy was scheduled a few days later. A complex tear of the medial meniscus extending to the articular surfaces was diagnosed. Partial meniscectomy was recommended. (This procedure usually takes about one hour—nonetheless, the preoperative preparation for general anesthesia and the postoperative recovery may add several hours to this time.) When Would You Have This Patient Report to the Hospital? The Day before Surgery or the Morning of Surgery? This patient should be hospitalized no later than the evening before surgery, given his history of frequent episodes of hypo- and hyperglycemia and his poor glycemic control. This should allow for final optimization of glucose control before surgery. Ideally, frequent con Continue reading >>
Hyperglycemic Crises In Diabetes
Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at ∼15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10). This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information. PATHOGENESIS Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). 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 to ketone bodies (β-hydroxybutyrate [β-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are in Continue reading >>
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Transitioning Safely From Intravenous To Subcutaneous Insulin
Current Diabetes Reports Authors Kathryn Evans Kreider, Lillian F. Lien Abstract The transition from intravenous (IV) to subcutaneous (SQ) insulin in the hospitalized patient with diabetes or hyperglycemia is a key step in patient care. This review article suggests a stepwise approach to the transition in order to promote safety and euglycemia. Important components of the transition include evaluating the patient and clinical situation for appropriateness, recognizing factors that influence a safe transition, calculation of proper SQ insulin doses, and deciding the appropriate type of SQ insulin. This article addresses other clinical situations including the management of patients previously on insulin pumps and recommendations for patients requiring glucocorticoids and enteral tube feedings. The use of institutional and computerized protocols is discussed. Further research is needed regarding the transition management of subgroups of patients such as those with type 1 diabetes and end-stage renal disease. Introduction Intravenous (IV) insulin is used in the hospitalized patient to control blood sugars for patients with and without diabetes who may exhibit uncontrolled hyperglycemia or for those who need close glycemic attention. Common hospital uses for IV insulin include the perioperative setting, during the use of high-risk medications (such as corticosteroids), or during crises such as diabetic ketoacidosis (DKA) [1,2]. Other conditions such as hyperglycemic hyperosmolar state (HHS) and trauma frequently require IV insulin, as well as specific hospital units such as the cardiothoracic intensive care unit [3,4]. The correlation between hyperglycemia and poor inpatient outcomes has been well described in the literature [5,6]. The treatment of hyperglycemia using an IV Continue reading >>
Guidelines For Management Of Dka
A. All pediatric patients with Diabetic Ketoacidosis (DKA) should be admitted to the hospital B. All pediatric DKA patients with initial HCO3- < 15 mEq/L, pH 7.2, a need for IV insulin infusion or clinical signs of shock should be admitted to the PICU. Classification of DKA Mild Moderate Severe Clinical Alert, well hydrated symptomatic (lethargic, vomiting, dehydrated, hyperventilating) somnolent, severely dehydrated or shocky Laboratory large ketones, pH => 7.30, HCO3- > 18 large ketones, pH 7.2 to 7.3, HCO3- 10 to 20 large ketones, pH < 7.2, HCO3- < 10 Treatment supplemental regular insulin SQ (0.1-0.2 units/kg q 4-6 hours) IV hydration IV insulin 0.1 units/kg/hour Admit to PICU IV hydration IV insulin 0.1 units/kg/hour Admit to PICU Management Initial Volume Expansion/Fluid Resuscitation Give 10 cc/kg 0.9% NaCl over 20 to 60 minutes (may need to be given faster). Poor perfusion, hypotension, or shock Give 20 cc/kg 0.9% NaCl over 20 to 60 minutes (time depends on amount of compromise) REASSESS If patient still shocky, give another 20 cc/kg NaCl over 20 to 60 minutes REASSESS Most patients will not require more than 20 cc/kg NaCl for initial rehydration, however some patients will need more. Frequent reassessment of patient's status will help guide fluid therapy. Too little fluid will hinder resolution of shock and acidosis, too much fluid may contribute to the development of cerebral edema. Often, very high glucose levels (> 500) and BUN > 30 mg/dL are indicative of severe dehydration. Maintenance IV fluids and rehydration Maintenance = 1500 to 2000 cc/m2/day or use cc/kg body weight (refer to Harriet Lane Handbook). May need to increase if patient is febrile or hyperventilating. For deficit replacement, assume at least a 10% dehydration (100 cc/kg) at admission. Give Continue reading >>
Diabetic Ketoacidosis Explained
Twitter Summary: DKA - a major complication of #diabetes – we describe what it is, symptoms, who’s at risk, prevention + treatment! One of the most notorious complications of diabetes is diabetic ketoacidosis, or DKA. First described in the late 19th century, DKA represented something close to the ultimate diabetes emergency: In just 24 hours, people can experience an onset of severe symptoms, all leading to coma or death. But DKA also represents one of the great triumphs of the revolution in diabetes care over the last century. Before the discovery of insulin in 1920, DKA was almost invariably fatal, but the mortality rate for DKA dropped to below 30 percent within 10 years, and now fewer than 1 percent of those who develop DKA die from it, provided they get adequate care in time. Don’t skip over that last phrase, because it’s crucial: DKA is very treatable, but only as long as it’s diagnosed promptly and patients understand the risk. Table of Contents: What are the symptoms of DKA? Does DKA occur in both type 1 and type 2 diabetes? What Can Patients do to Prevent DKA? What is DKA? Insulin plays a critical role in the body’s functioning: it tells cells to absorb the glucose in the blood so that the body can use it for energy. When there’s no insulin to take that glucose out of the blood, high blood sugar (hyperglycemia) results. The body will also start burning fatty acids for energy, since it can’t get that energy from glucose. To make fatty acids usable for energy, the liver has to convert them into compounds known as ketones, and these ketones make the blood more acidic. DKA results when acid levels get too high in the blood. There are other issues too, as DKA also often leads to the overproduction and release of hormones like glucagon and adrenaline Continue reading >>
Management Of Adult Diabetic Ketoacidosis
Go to: Abstract Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Go to: Introduction In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion US dollars. Omission of insulin is the most common precipitant of DKA.2,3 Infections, acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke) and gastrointestinal tract (bleeding, pancreatitis), diseases of the endocrine axis (acromegaly, Cushing’s syndrome), and stress of recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hor Continue reading >>
Perioperative Management Of The Diabetic Patient
Overview Diabetes mellitus (DM) is an increasingly common medical condition affecting approximately 8% of the population of the United States. Of these 25 million people, it is estimated that nearly 7 million are unaware that they have the disease until faced with associated complications. [1, 2] The prevalence of DM is even greater in hospitalized patients. The American Diabetes Association conservatively estimates that 12-25% of hospitalized adult patients have diabetes mellitus (DM). With the increasing prevalence of diabetic patients undergoing surgery, and the increased risk of complications associated with diabetes mellitus, appropriate perioperative assessment and management are imperative. An estimated 25% of diabetic patients will require surgery. Mortality rates in diabetic patients have been estimated to be up to 5 times greater than in nondiabetic patients, often related to the end-organ damage caused by the disease. Chronic complications resulting in microangiopathy (retinopathy, nephropathy, and neuropathy) and macroangiopathy (atherosclerosis) directly increase the need for surgical intervention and the occurrence of surgical complications due to infections and vasculopathies. [3, 4, 5, 6] Infections account for 66% of postoperative complications and nearly one quarter of perioperative deaths in patients with DM. Data suggest impaired leukocyte function, including altered chemotaxis and phagocytic activity. Tight control of serum glucose is important to minimize infection. In addition to postoperative infectious complications, postoperative myocardial ischemia is increased among patients with DM undergoing cardiac and noncardiac surgery. [7, 8, 9] Fortunately, tighter glycemic control has been shown to have a profound effect on reducing the incidence of m Continue reading >>
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 >>
Targets For Protective Action Of Insulin
fuel and energy metabolism glucose free fatty acids reactive oxygen species nutritional status coagulation pathway inflammatory pathway endothelium protection against vessel wall inflammatory processes vasodilatory action heart host defenses against infection Noncritically ill Fasting glucose < 126 mg /dL and all random glucoses < 180 - 200 mg /dL Critically ill Blood glucose levels should be kept as close to 110 mg /dL as possible and generally < 140 mg /dL These patients require an intravenous insulin protocol that has demonstrated efficacy and safety in achieving the desired glucose range without increasing risk for severe hypoglycemia Deciding whether to maintain the ambulatory treatment plan in the hospital 8 12 6 10 The Pattern of Insulin Requirement during Normal Health, Meal Plan, and Activity is Not Necessarily Reproduced in the Hospital Scheduled subcutaneous insulin Which pattern of carbohydrate exposure describes the patient ? Discrete meals Negligible carbohydrate Continuous carbohydrate exposure Transitional meal plan / grazing Daytime grazing / overnight enteral feedings Constructing a profile for scheduled subcutaneous insulin …. 6 pm 12 am 6 am 12 pm Glargine NPH SQ Regular Lispro / Aspart / Glulisine Requirement for exogenous insulin during prolonged fasting may disappear in type 2 DM, but even during prolonged fasting it is absolute in type 1 DM type 1 DM type 2 DM requirement for exogenous basal insulin vs time fasting A Bad Practice: 70/30 Insulin plus Sliding Scale Scheduled or routine 0800 & 1700 Q4HRS, or 0200, 0600, 1000, 1400, 1800, 2200 This means 8 shots daily. There is a risk of stacking, & BG tests fail to synchronize: 0200, 0600, 0800, 1000, 1400, 1700, 1800, 2200 Sample “consistent carbohydrate†meal plan order with � Continue reading >>
Boost Your Confidence In Caring For Patients With Insulin Pumps
Beth T, age 42, is a Caucasian female with a 32-year history of type 1 diabetes and a 15-year history of Crohn’s disease. For the last 12 years, she has been using a continuous subcutaneous insulin pump; her most recent hemoglobin A1c value was 5.7%. When she arrives in the emergency department at 9 am with a possible GI bleed, her blood glucose (BG) level is 98 mg/dL. At 9:45 am, the attending physician removes her insulin pump and orders sliding-scale insulin with insulin lispro, a rapid-acting analog insulin. He also orders point-of-care BG testing before meals and at bedtime, a clear liquid diet, and a gastroenterology consultation. At 10:15 am, the gastroenterologist puts Beth on nothing-by-mouth (NPO) status and schedules a colonoscopy for the next day. When she arrives on your med-surg unit at 1 pm, you review the orders and feel relieved that her insulin pump has been removed, because you don’t know much about these pumps. You plan to check her BG at 6 pm—the next scheduled time. But at 4:45, Beth expresses concern about her BG level. She tells you she has been taught never to remove her pump for more than an hour or two. She says she feels “out of it” and has been urinating more frequently since the pump was removed. When you notice her breath odor is foul and her breathing is rapid and deep, you check her BG—and become alarmed when you see it’s 512 mg/dL. You note she’s experiencing signs and symptoms of diabetic ketoacidosis (DKA). You ask yourself, “How did this happen?” Continuous subcutaneous insulin infusion (CSII) pump therapy is an effective self-management tool for patients with diabetes. It has been linked to decreased hemoglobin A1c levels and improved satisfaction with diabetes self-management. More than 300,000 Americans current Continue reading >>
Management Of Diabetes Mellitus In Hospitalized Patients
INTRODUCTION Patients with type 1 or type 2 diabetes mellitus are frequently admitted to a hospital, usually for treatment of conditions other than the diabetes [1,2]. In one study, 25 percent of patients with type 1 diabetes and 30 percent with type 2 diabetes had a hospital admission during one year; patients with higher values for glycated hemoglobin (A1C) were at highest risk for admission [2]. The prevalence of diabetes rises with increasing age, as does the prevalence of other diseases; both factors increase the likelihood that an older person admitted to a hospital will have diabetes. The treatment of patients with diabetes who are admitted to the general medical wards of the hospital for a procedure or intercurrent illness is reviewed here. The treatment of hyperglycemia in critically ill patients, the perioperative management of diabetes, and the treatment of complications of the diabetes itself, such as diabetic ketoacidosis, are discussed separately. (See "Glycemic control and intensive insulin therapy in critical illness" and "Perioperative management of blood glucose in adults with diabetes mellitus" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment" and "Management of hypoglycemia during treatment of diabetes mellitus".) GOALS IN THE HOSPITAL SETTING The main goals in patients with diabetes needing hospitalization are to minimize disruption of the metabolic state, prevent adverse glycemic events (especially hypoglycemia), return the patient to a stable glycemic balance as quickly as possible, and ensure a smooth transition to outpatient care. These goals are not always easy to achieve. On the one hand, the stress of the acute illness tends to raise blood glucose concentrations. On the other hand, the anorexia that often a Continue reading >>
1. Start Iv Fluids (1 L Of 0.9% Nacl Per Hr Initially) 2. If Serum K+ Is <3.3 Meq/l Hold Insulin
DKA Diagnostic Criteria (See page 3 for more details):  Blood glucose >250 mg/dl,  Arterial pH <7.3,  Bicarbonate ≤18 mEq/l,  Anion Gap Acidosis  Moderate ketonuria or ketonemia.  Give 40 mEq/h until K ≥ 3.3 mEq/L 3. Initiate DKA Order Set Phase I 4. Start insulin 0.14 units/kg/hr IV infusion (calculate dose) RN will titrate per DKA protocol Insulin Potassium Bicarbonate IVF Look for the Cause - Insulin deficiency - Infection/Inflammation (PNA, UTI, pancreatitis, cholecystitis) - Ischemia/Infarction (myocardial, cerebral, gut) - Intoxication (EtOH, drugs) - Iatrogenic (drugs, lack of insulin) - Pregnancy DKA/HHS Pathway Phase 1 (Adult) Approved by Diabetes Steering Committee, MMC, 2015 Initiate and continue insulin gtt until serum glucose reaches 250 mg/dl. RN will titrate per protocol to achieve target. When sugar < 250 mg/dl proceed to DKA Phase II (reverse side) DKA/HHS Pathway Phase 2 (Adult) Non-ICU Patients Phase 2: Blood sugar now less than 250mgd/dl. If Anion Gap Normalized* If Anion Gap Elevated* Critical Illness (ICU) Follow guidelines to the right when gap has normalized.* Approved by Glycemic Steering Committee, MMC, 2015  Transition to DKA Order Set Phase 2  Discontinue Phase 1 insulin infusion order and DKA nursing titration protocol from phase 1.  Change to fixed dose insulin infusion at suggested rate of 2.5 units/hr (Adjust as needed for individual patient with typical dose range of 0.02 to 0.05 units/kg/hr based on drip rate and response in phase 1). Do not discontinue insulin therapy.  Start dextrose containing IV fluid such as D5 ½ NS and adjust dextrose to goal blood sugar 150- 200.  Continue to check labs regularly.  Reevaluate for underlying causes a Continue reading >>
Treatment Of Dka
GOAL: Replacement of fluid, insulin and electrolytes. Correction of hyperosmolarity (hyperglycemia) and acidosis. Avoid complications of therapy. DIAGNOSIS: 1. Serum glucose > 250 mg/dl 2. Serum bicarbonate < 20 mEq/L 3. Ketonemia PRESENTATION: 1. New Onset DM: polyuria, polydipsia, weight loss, nausea, vomiting, hyperpnea (increased depth of respiration), abdominal pain, dehydration, coma. 2. Known diabetic: hyperglycemia, ketonuria, polyuria, hyperpnea and any of the above. MANAGEMENT: 1. Draw initial labs: VBG, capillary BG, electrolytes, glucose, BUN, creatinine, serum ketones, Ca, Mg, P, UA, ± CBC a. Hyponatremia: Usually factitious. Corrected Na (mg/dl) = Serum Na + 1.6 (Serum glucose-100) 100 b. Potassium: Artificially elevated. During acidosis, K+ is exchanged for H+. Patients are usually total body K+ depleted and serum K+ levels will drop rapidly with correction of acidosis. c. Creatinine: May be artificially elevated in some labs (secondary to ketonemia). d. pH: May be 6.8-7.29; cannot predict rapidity of response from initial pH. e. White Blood Cell count: Usually elevated with leukocytosis f. Serum lipids: High triglycerides 2. Begin fluid resuscitation: Give normal saline at 10-20 cc/kg over next 1 or 2 hours. This will lower serum glucose but will not correct acidosis (may actually worsen as hydration results in redistribution of lactic acid). 3. Begin flow sheet: Should have hourly vital signs, neuro checks, Is and Os, and accurately calculated nets I/O at least every 4 hours to make sure you are ahead on fluids. 4. Keep patient NPO. 5. Detailed H & P: Evaluate regarding possible source of infection may have precipitated DKA (urine, lungs, sinuses, otitis, skin, blood, CNS) and treat if needed. Ask about insulin storage (left in car), age of bottles. Continue reading >>
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Mind The Gap: A Nurses' Map To Understanding And Managing Dka
Sep 26, 2014 ... Clinical Nurse Specialist. Cleveland Clinic Respiratory ... will be able to describe the physiology of DKA ... Diabetes. Usually associated with: Type II Diabetes. DKA results from an .... In Current Medical Diagnosis &. Treatment. Mind the Gap: Navigating the Underground World of DKA Christina Canfield, MSN, RN, ACNS-BC, CCRN Clinical Nurse Specialist Cleveland Clinic Respiratory Institute Objectives • Upon completion of this activity the learner will be able to describe the physiology of DKA • Upon completion of this activity the learner will be able to describe the nurse’s role in treatment strategies for DKA Back That Train Up! • Insulin has a number of effects on glucose metabolism, including: – Inhibition of glycogenolysis and gluconeogenesis • Insulin hits the breaks on extra glucose conversion or production – Increased glucose transport into fat and muscle • Insulin takes glucose on a sweet ride into the fat and muscle – Increased glycolysis in fat and muscle • Insulin fuels the generation of ATP – Stimulation of glycogen synthesis • Insulin parks the glucose train at the station until it’s needed 1 9/26/2014 So what causes DKA? How do you know you’re on the right train? Diabetic Keto Acidosis Type I Diabetes DKA results from an insulin deficiency; in response the body switches to burning fatty acids and producing acidic ketone bodies Hyperosmolar Hyperglycemic State Usually associated Type II Diabetes with: >250 Plasma glucose (mg/dL) >600 7.3 18 + Urine Ketones Small + Serum Ketones < 0.6mmol/L Variable Serum Osmolality >10-12 Anion Gap >320 HHS results from an insulin deficiency that leads to a serum glucose that is usually higher 600 mg/dl, and a resulting high serum osmolality Variable Insulin deficiency PHYSIOLO Continue reading >>
