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Why Is Potassium Given In Diabetic Ketoacidosis?

Board Review: Diabetic Ketoacidosis And Total Body Potassium

Board Review: Diabetic Ketoacidosis And Total Body Potassium

A 23 y/o M with a PMHx of Type 1 DM arrives to your ED reporting nausea, vomiting and elevated blood sugars on his home monitor. His initial blood work indicates he is in DKA. For which of the following potassium levels should initiation of an insulin drip be delayed for potassium repletion? (scroll down for the answer) a) < 3.0 mEq/L b) < 3.3 mEq/L c) < 3.5 mEq/L d) < 3.8 mEq/L e) < 4.0 mEq/L The correct answer is b) < 3.3 mEq/L Following the American Diabetes Association guidelines for the treatment of DKA, patients with hypokalemia on initial labs of 3.3 mEq/L or less must have potassium replacement with a delay in insulin treatment until the potassium concentration is restored to > 3.3 mEq/L Patients in DKA are low in total body potassium and their serum concentration is falsely elevated due to extracellular shift. On average, patients will have a potassium deficit of 3-5 mEq/kg. Treatment with insulin will cause a shift of potassium intracellularly which can lead to severe hypokalemia and cardiac dysrhythmia. All DKA patients will require potassium replacement to prevent hypokalemia. Generally 20mEq of potassium in each liter of fluid given will maintain a normal serum potassium concentration. The ADA Guidelines for DKA can be found here: A Core review of Hypokalemia in the ED was recently posted on emDOCs by Dr. Swaminathan, see it here: Continue reading >>

Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis

Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis

Go to: Abstract Hypokalemia is common during the treatment of diabetic ketoacidosis (DKA); however, severe hypokalemia at presentation prior to insulin treatment is exceedingly uncommon. A previously healthy 8-yr-old female presented with new onset type 1 diabetes mellitus, severe DKA (pH = 6.98), and profound hypokalemia (serum K = 1.3 mmol/L) accompanied by cardiac dysrhythmia. Insulin therapy was delayed for 9 h to allow replenishment of potassium to safe serum levels. Meticulous intensive care management resulted in complete recovery. This case highlights the importance of measuring serum potassium levels prior to initiating insulin therapy in DKA, judicious fluid and electrolyte management, as well as delaying and/or reducing insulin infusion rates in the setting of severe hypokalemia. Keywords: diabetic ketoacidosis, hypokalemia, insulin, low-dose insulin drip, pediatric Nearly one third of children with newly diagnosed type 1 diabetes present in diabetic ketoacidosis (DKA). Higher proportions of young children and those from disadvantaged socioeconomic groups present with DKA (1). DKA is the leading cause of mortality among children with diabetes, and electrolyte abnormalities are a recognized complication of DKA contributing to morbidity and mortality (2, 3). Total body potassium deficiency of 3-6 mEq/kg is expected at presentation of DKA due to osmotic diuresis, emesis, and secondary hyperaldosteronism; however, pretreatment serum potassium levels are usually not low due to the extracellular shift of potassium that occurs with acidosis and insulin deficiency (3, 4). After insulin treatment is initiated, potassium shifts intracellularly and serum levels decline. Replacement of potassium in intravenous fluids is the standard of care in treatment of DKA to prevent Continue reading >>

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What causes potassium and sodium loss in diabetic ketoacidosis (DKA)? Glucosuria leads to osmotic diuresis, dehydration and hyperosmolarity. Severe dehydration, if not properly compensated, may lead to impaired renal function. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. The most characteristic disturbance is total body potassium loss. This loss is not mirrored in serum potassium levels, which may be low, within the reference range, or even high. Potassium loss is caused by a shift of potassium from the intracellular to the extracellular space in an exchange with hydrogen ions that accumulate extracellularly in acidosis. Much of the shifted extracellular potassium is lost in urine because of osmotic diuresis. Patients with initial hypokalemia are considered to have severe and serious total body potassium depletion. High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia. Sodium also is lost in the urine during the osmotic diuresis. 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. 2012 Jan. 29(1):32-5 Continue reading >>

[full Text] Correlation Of Acidosis-adjusted Potassium Level And Cardiovascular Ou | Dmso

[full Text] Correlation Of Acidosis-adjusted Potassium Level And Cardiovascular Ou | Dmso

The protocol was registered with PROSPERO (Registration Number: CRD42018098772). An article was included if it met the following criteria: 1) the study reported the prevalence of DKA in adult diabetic patients and assessed admission potassium level and pH; 2) the study qualitatively observed cardiovascular outcomes in DKA patients; 3) the design of the study was a cross-sectional or cohort, or randomized controlled trial. Studies were excluded if 1) it was a case-control, case report, conference proceeding, systematic review, letter to editor, an opinion, or research brief; 2) published in languages other than English; 3) reported DKA secondary to pregnancy or among pediatrics, or 4) studies evaluating therapeutic intervention which includes DKA secondary to sodium-glucose co-transporter 2 inhibitor. Level of serum potassium, and pH-adjusted corrected level of potassium at the time of admission. Cardiovascular outcomes in relation to potassium in DKA episode Specifically, the CV outcomes were noted in relation to the level of potassium at the time of occurrence of CV event and included ECG, report of fibrillation, tachycardia or bradycardia, central venous pressure, cardiac arrest, myocardial infarction, and troponin. Moreover, reports of CV outcomes or signs and symptoms were recorded if the CV outcome was reported as the reason for fatality. It was further noted if any relationship was given by the authors between hypokalemia and the reason for such CV outcome. All references retrieved were initially grouped under the respective search engine. Duplicates were removed, and titles were screened for eligibility. After removal of irrelevant studies, regrouping was done according to the nature of the study, ie, case series, clinical trial, guideline, etc. Relevant demogra Continue reading >>

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Understand the management of patients with diabetic ketoacidosis and other hyperglycemic emergencies. ​ The acute onset of hyperglycemia with attendant metabolic derangements is a common presentation in all forms of diabetes mellitus. The most current data from the National Diabetes Surveillance Program of the Centers for Disease Control and Prevention estimate that during 2005-2006, at least 120,000 hospital discharges for diabetic ketoacidosis (DKA) occurred in the United States,(1) with an unknown number of discharges related to hyperosmolar hyperglycemic state (HHS). The clinical presentations of DKA and HHS can overlap, but they are usually separately characterized by the presence of ketoacidosis and the degree of hyperglycemia and hyperosmolarity, though HHS will occasionally have some mild degree of ketosis. DKA is defined by a plasma glucose level >250 mg/dL, arterial pH <7.3, the presence of serum ketones, a serum bicarbonate measure <18 mEq/L, and a high anion gap metabolic acidosis. The level of normal anion gap may vary slightly by individual institutional standards. The anion gap also needs to be corrected in the presence of hypoalbuminemia, a common condition in the critically ill. Adjusted anion gap = observed anion gap + 0.25 * ([normal albumin]-[observed albumin]), where the given albumin concentrations are in g/L; if given in g/dL, the correction factor is 2.5.(3) HHS is defined by a plasma glucose level >600 mg/dL, with an effective serum osmolality >320 mOsm/kg. HHS was originally named hyperosmolar hyperglycemic nonketotic coma; however, this name was changed because relatively few patients exhibit coma-like symptoms. Effective serum osmolality = 2*([Na] + [K]) + glucose (mg/dL)/18.(2) Urea is freely diffusible across cell membranes, thus it will Continue reading >>

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

Successful Use Of Renal Replacement Therapy For Refractory Hypokalemia In A Diabetic Ketoacidosis Patient

Successful Use Of Renal Replacement Therapy For Refractory Hypokalemia In A Diabetic Ketoacidosis Patient

Volume 2019 |Article ID 6130694 | 3 pages | Successful Use of Renal Replacement Therapy for Refractory Hypokalemia in a Diabetic Ketoacidosis Patient 1Department of Medicine, Saint Josephs University Medical Center, 703 Main St, Paterson, NJ, USA 2New York Medical College, Valhalla, NY, USA A 39-year-old African-American female presented to the emergency department with a seven-day history of right upper quadrant abdominal pain accompanied by nausea, vomiting, and diarrhea. She was noted to be alert and following commands, but tachypneic with Kussmaul respirations; and initial laboratory testing supported a diagnosis of diabetic ketoacidosis (DKA) and hypokalemia. To avoid hypokalemia-induced arrhythmias, insulin administration was withheld until a serum potassium (K) level of 3.3 mEq/L could be achieved. Efforts to increase the patients potassium level via intravenous repletion were ineffectual; hence, an attempt was made at more aggressive potassium repletion via hemodialysis using a 4 mEq/L K dialysate bath. The patient was started on Aldactone and continuous veno-venous hemodialysis (CVVH) with ongoing low-dose insulin infusion. This regimen was continued over 24 h resulting in normalization of the patients potassium levels, resolution of acidosis, and improvement in mental status. Upon resolution of her acidemia, the patient was transitioned from insulin infusion to treatment with a subcutaneous insulin aspart and insulin detemir, and did not experience further hypokalemia. Considering our success, we propose CVVH as a tool for potassium repletion when aggressive intravenous (IV) repletion has failed. Hospitalizations for diabetic ketoacidosis (DKA) have soared in incidence over the recent years, increasing 54.9% from 19.5 to 30.2 hospitalizations per 1,000 people Continue reading >>

Hyperkalaemia In Diabetic Ketoacidosis

Hyperkalaemia In Diabetic Ketoacidosis

Dear Editor, I have a brief comment on the informative ‘Lesson of the week’ by Moulik and colleagues, describing an association between hyperkalaemia and an ECG pattern suggesting acute myocardial infarction in a patient with diabetic ketoacidosis (DKA). One of the mechanisms of hyperkalaemia in DKA stated at the beginning of the Discussion is not strictly correct. It is inorganic acids, and not organic acids (including lactic acid), that cause hyperkalaemia as a result of potassium ions leaving cells in ‘exchange’ for hydrogen ion entry (and their intracellular buffering). In DKA, the key mechanism is lack of insulin, which is probably the most important short-term regulator of plasma potassium concentration (through stimulation of the cell ‘sodium’ pump – Na,K-ATPase) and defence against acute hyperkalaemia resulting from our daily intake of potassium (~80 mmol): The extracellular pool of potassium is around 65 mmol and could almost double after a single steak meal (~50 mmol), which is too rapid a change for compensatory renal excretion. In DKA, an additional mechanism is the osmotic shrinkage of cells as a result of the high plasma glucose concentration (and plasma osmolality), which steepens the intracellular to extracellular potassium concentration gradient and thereby causes an increase in potassium ion loss from cells. Of course, these observations do not materially alter the management of DKA, but only serve to emphasise the importance of inulin administration, glucose control and re-salination over the use (though not excluding it in severe metabolic acidosis) of bicarbonate, bearing in mind that such patients have usually become potassium depleted as a consequence of earlier increased renal losses, and therefore risk developing significant hypoka 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In 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 >>

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

We started an intravenous insulin infusion and hemodialysis to reduce the glucose and potassium levels. Fluid infusions were not given because there was no evidence of a fluid deficit. Four hours after beginning treatment, the plasma glucose was gradually reduced from 1498 to around 400 mg/dL, and serum potassium decreased from 9.0 to 4.0 mEq/L. The hyperkalemic changes disappeared from ECG. On hospital day 2, however, his right hemiplegia persisted. Head computed tomography demonstrated a low-density area in the left frontal lobe, indicating a left frontal cerebral infarction. After glycemic control, serum sodium level normalized to baseline level (135140 mEq/L). Although the insulin pump tube was fully filled with insulin, the infusion line was not properly placed into the abdominal skin. The patient underwent rehabilitation, but he was unable to manage his insulin pump because of the hemiplegia and higher cortical dysfunction induced by the cerebral infarction. We therefore removed the pump and switched to intermittent insulin therapy. We performed brain CT scan twice, and there were no progression of the infarct area and brain edematous findings. On hospital day 40, he was transferred to another hospital for further rehabilitation. In patients with anuria on hemodialysis, DKA is generally rare, because urinary loss of water and electrolytes does not occur and regular hemodialysis improves metabolic acidosis ( 2 ). In this patient, extreme hyperkalemia of 9.0 mEq/L with typical hyperkalemic ECG changes was observed. In general, hyperglycemia is positively correlated with the serum potassium level ( 3 ), but hyperkalemia to this extreme degree is rare. Lack of insulin action does not produce hyperglycemia alone but also causes potassium to shift from the intracellula Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>

Initial Potassium Replacement In Diabetic Ketoacidosis: The Unnoticed Area Of Gap

Initial Potassium Replacement In Diabetic Ketoacidosis: The Unnoticed Area Of Gap

Initial Potassium Replacement in Diabetic Ketoacidosis: The Unnoticed Area of Gap We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Initial Potassium Replacement in Diabetic Ketoacidosis: The Unnoticed Area of Gap Diabetic ketoacidosis is an acute complication of diabetes mellitus (DM). It affects all the types of DM and hence is a continuous threat for all the diabetes patients ( 1 ). DKA is a well-studied disease. Among the precipitating causes, mostly reported factors are non-compliance of patients with the antidiabetic treatment, and infection; others, however, may not have any precipitating cause ( 1 , 2 ). The progress of disease is very simple; lack of insulin causes hyperglycemia and inability of glucose to enter the cell. In-turn, triglycerides are broken down to free fatty acids which are used as a source of energy ( 1 , 3 , 4 ). In due process, the end-product of this metabolic derangement, i.e., ketones, cause acidification of blood causing major disruption in homeostasis. Similar to pathophysiology, the treatment of DKA is also simple and encompasses administration of insulin to achieve euglycaemia, and administration of crystalloid or colloidal solution to attain euvolaemia and euelectrolytaemia ( 1 3 ). Nevertheless, by the time patient reports for medical attention, these simple derangements and the rectification pathway have had gone significant derailment with potassium being the most affected ion throughout the Continue reading >>

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

Approach Considerations Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis. It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>

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