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Why Does Metabolic Acidosis Cause Abdominal Pain

Metabolic Acidosis; Gap Positive

Metabolic Acidosis; Gap Positive

Metabolic acidosis is defined by low serum pH (less than 7.35-7.45) and low serum bicarbonate. It occurs by one of three major mechanisms: 1. Increased endogenous acid (i.e., lactic acidosis, diabetic ketoacidosis). 2. Decreased renal acid excretion (i.e., renal failure). In determining the underlying etiology for a metabolic acidosis, the serum anion gap must be calculated by subtracting the major measured anions (chloride and bicarbonate) from the major measured cation (sodium). If the result is greater than 12 meq/L (which is the normal value for most laboratories), the acidosis is said to be an anion gap acidosis. The expected anion gap should is lower in hypoalbuminemia and should be corrected - for each decrease of 1gm/dl in albumin, the normal anion gap should be decreased by approximately 2.5 meq/L. A. What is the differential diagnosis for this problem? Anion gap acidosis can be the result from: 1. A fall in unmeasured cations (as seen in hypomagnesemia or hypocalcemia). The most common reasons for a rise in anions are ingestions, lactic acidosis, ketoacidosis and renal failure. Ingestions of multiple different toxins can result in unmeasured anions causing a metabolic gap acidosis. Most commonly salicylate and the alcohols (methanol and ethylene glycol) can lead to severe acidosis. The inhalant toluene may also be a culprit. Lactic acidosis is the most common cause of an elevated anion gap acidosis in hospitalized patients, occurring with decreased perfusion causing relative tissue ischemia. This leads to increased lactic acid production and impaired renal excretion with resultant acid accumulation (Type A lactic acidosis). Type B lactic acidosis occurs in patients without overt tissue and can be seen in diabetics on metformin, patients with hematologic and s Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Anion Gap (elevated) Differential Diagnosis

Anion Gap (elevated) Differential Diagnosis

Acetaminophen Alcoholic Ketoacidosis Diabetic Ketoacidosis Ethylene Glycol Iron Isoniazid Lactic Acidosis Metformin Methanol Paraldehyde Salicylates Related Content Editors & Reviewers Normal Anion Gap: 8 - 12 +/- 2 Associations: Glucose levels > 250 mg/dL +/- abdominal pain +/- nausea & vomiting + ketones in the urine + serum bicarbonate < 18 Pathophysiology: Insufficient presence of insulin that results in the abnormal breakdown of fatty acids that generate ketoacids. Associations: History of tuberculosis (latent or active) Pathophysiology: Due to functional deficiencies in pyridoxine (vitamin B6) that can serve as a co-factor in metabolic reactions. This leads to a metabolic acidosis. Associations: Numerous medical conditions or drugs containing propylene glycol (lorazepam; phenytoin) Pathophysiology: Lactic acid formation is a byproduct of another underlying problem that prevents its metabolism or prevent pyruvate from entering the Krebs cycle. Associations: Reports of ingestion/Suicide Attempt (or) elderly patient on chronic aspirin +/- mixed acid/base disorder Pathophysiology: Initially stimulates the medullary center in the brain and causes increased respirations leading to respiratory alkalosis. Then shifts to a metabolic acidosis and uncoupling of cellular respiration. Continue reading >>

Systemic Causes Of Abdominal Pain

Systemic Causes Of Abdominal Pain

a Department of Emergency Medicine, Thomas Jefferson University Hospital, 1020 Sansom Street, Thompson Building 239, Philadelphia, PA 19107, USA b Division of Emergency Ultrasonography, Department of Emergency Medicine, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, PA 19104, USA Abstract A variety of systemic and extra-abdominal diseases can cause symptoms within the abdominal cavity. Systemic and extra-abdominal diseases may include abdominal symptoms caused by several mechanisms. This article discusses the most important and common of these causes, namely the metabolic/endocrine causes, hematologic causes, inflammatory causes, infectious causes, functional causes, and the neurogenic causes. Keywords A variety of systemic and extra-abdominal diseases can cause symptoms within the abdominal cavity (Box 1). This article discusses the most important and common of these diseases. Systemic and extra-abdominal diseases may include abdominal symptoms caused by several mechanisms listed in Table 1. Mechanisms include direct pathologic effects on intra-abdominal organs (eg, gallstone formation in sickle cell disease); conversely, systemic illnesses (eg, congestive heart failure, diabetic ketoacidosis [DKA], or addisonian crisis) may themselves be precipitated by diseases in the abdomen. Some systemic illnesses have a direct (eg, constipation in hypercalcemia) or indirect (eg, nausea and vomiting in diabetic or alcoholic ketoacidosis [AKA]) effect on the functioning of the gastrointestinal (GI) tract. Abdominal symptoms may be caused by disease in contiguous organs outside the abdomen (eg, diaphragmatic irritation from disease of adjacent structures in the lung and mediastinum).1–4 Finally, symptoms may be referred to the abdomen from extra-abdom Continue reading >>

Acid-base Imbalances: Metabolic Acidosis And Alkalosis

Acid-base Imbalances: Metabolic Acidosis And Alkalosis

Acid-Base Imbalances: Metabolic Acidosis and Alkalosis; Respiratory Acidosis and Alkalosis The hydrogen ion concentration ([H+]) of the body, described as the pH or negative log of the [H+], is maintained in a narrow range to promote health and homeostasis. The body has many regulatory mechanisms that counteract even a slight deviation from normal pH. An acid-base imbalance can alter many physiological processes and lead to serious problems or, if left untreated, to coma and death. A pH below 7.35 is considered acidosis and above 7.45 is alkalosis. Alterations in hydrogen ion concentration can be metabolic or respiratory in origin or they may have a mixed origin. Metabolic acidosis, a pH below 7.35, results from any nonpulmonary condition that leads to an excess of acids over bases. Renal patients with chronic acidemia may show signs of skeletal problems as calcium and phosphate are released from bone to help with the buffering of acids. Children with chronic acidosis may show signs of impaired growth. Metabolic alkalosis, a pH above 7.45, results from any nonpulmonary condition that leads to an excess of bases over acids. Metabolic alkalosis results from one of two mechanisms: an excess of bases or a loss of acids. Patients with a history of congestive heart failure and hypertension who are on sodium-restricted diets and diuretics are at greatest risk for metabolic alkalosis. Metabolic alkalosis can also be caused by prolonged vomiting, hyperaldosteronism, and diuretic therapy. Respiratory acidosis is a pH imbalance that results from alveolar hypoventilation and an accumulation of carbon dioxide. It can be classified as either acute or chronic. Acute respiratory acidosis is associated with a sudden failure in ventilation. Chronic respiratory acidosis is seen in patient Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea Continue reading >>

Mala: Metformin-associated Lactic Acidosis

Mala: Metformin-associated Lactic Acidosis

By Charles W. O’Connell, MD Introduction Metformin is a first-line agent for type 2 diabetes mellitus often used as monotherapy or in combination with oral diabetic medications. It is a member of the biguanide class and its main intended effect is expressed by the inhibition of hepatic gluconeogenesis. In addition, metformin increases insulin sensitivity, enhances peripheral glucose utilization and decreases glucose uptake in the gastrointestinal tract. Phenformin, a previously used biguanide, as withdrawn from the market in the 1970’s due its association with numerous cases of lactic acidosis. Metformin is currently used extensively in the management of diabetes and is the most commonly prescribed biguanide worldwide. The therapeutic dosage of metformin ranges from 850 mg to a maximum of 3000 mg daily and is typically divided into twice daily dosing. It is primarily used in the treatment of diabetes but has been used in other conditions associated with insulin resistance such as polycystic ovarian syndrome. MALA is a rare but well reported event that occurs with both therapeutic use and overdose states. Case presentation A 22-year-old female presents to the Emergency Department after being found alongside a suicide note by her family. She was thought to have taken an unknown, but large amount of her husband’s metformin. She arrives at the ED nearly 10 hours after ingestion. She was agitated, but conversant. She reports having nausea and vague feelings of being unwell and is very distraught over the state of her critically ill husband. She has some self-inflicted superficial lacerations over her left anterior forearm. Her vital assigns upon arrival were: T 98.9 degrees Fahrenheit, HR initially 140 bpm which improved to 110 bpm soon after arrival, BP 100/50, RR 22, Continue reading >>

Understanding The Presentation Of Diabetic Ketoacidosis

Understanding The Presentation Of Diabetic Ketoacidosis

Hypoglycemia, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) must be considered while forming a differential diagnosis when assessing and managing a patient with an altered mental status. This is especially true if the patient has a history of diabetes mellitus (DM). However, be aware that the onset of DKA or HHNS may be the first sign of DM in a patient with no known history. Thus, it is imperative to obtain a blood glucose reading on any patient with an altered mental status, especially if the patient appears to be dehydrated, regardless of a positive or negative history of DM. In addition to the blood glucose reading, the history — particularly onset — and physical assessment findings will contribute to the formulation of a differential diagnosis and the appropriate emergency management of the patient. Pathophysiology of DKA The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA. Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are rece Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com 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 >>

Non-surgical Causes Of Acute Abdominal Pain

Non-surgical Causes Of Acute Abdominal Pain

Non-Surgical Causes of Acute Abdominal Pain Abdominal pain constitutes 5% of the causes of emergency admissions and is an important part in the practice of emergency services in all centers. Patients may suffer from acute surgical abdomen, acute abdomen with nonsurgical diseases or acute problems of chronic diseases. Abdominal pain is sometimes associated with acute trauma. Clinical assessment is a process where diagnosis and treatment must be done quickly and must be well managed. We have tried here to discuss the non-surgical causes of abdominal pain. 1. Introduction Acute abdomen describes the sudden and severe starting of abdominal pain with unexplained etiology [1]. Case management should be done fairly quickly. Nonsurgical diseases as well as surgical pathologies could be the cause of acute abdomen. Medical history and physical examination findings are very important for assessment. Abdominal pain is the most important sign of acute abdomen but might not be observed in each cases [2]. Especially the elderly and children should be considered for acute abdomen. Abdominal pain is usually a feature, but a pain-free acute abdomen can occur, particularly in older people, in children, in the immunocompromised, and in the women during their last trimester of pregnancy. Acute abdominal complaints are common [3]. The differential diagnosis of acute abdomen should be done as soon as possible with the medical history, physical examination, laboratory and radiological findings; and the diagnosis should be accelerated for patient management [4]. 2. Pathophysiology 2.1. Visceral pain Visceral pain is a kind of a pain resulting from abdominal, pelvic and thoracic organs whose mechanism is not clearly understood and thus, very difficult to identify [5]. Visceral pain is a common, Continue reading >>

Cardiovascular Complications Of Ketoacidosis

Cardiovascular Complications Of Ketoacidosis

US Pharm. 2016;41(2):39-42. ABSTRACT: Ketoacidosis is a serious medical emergency requiring hospitalization. It is most commonly associated with diabetes and alcoholism, but each type is treated differently. Some treatments for ketoacidosis, such as insulin and potassium, are considered high-alert medications, and others could result in electrolyte imbalances. Several cardiovascular complications are associated with ketoacidosis as a result of electrolyte imbalances, including arrhythmias, ECG changes, ventricular tachycardia, and cardiac arrest, which can be prevented with appropriate initial treatment. Acute myocardial infarction can predispose patients with diabetes to ketoacidosis and worsen their cardiovascular outcomes. Cardiopulmonary complications such as pulmonary edema and respiratory failure have also been seen with ketoacidosis. Overall, the mortality rate of ketoacidosis is low with proper and urgent medical treatment. Hospital pharmacists can help ensure standardization and improve the safety of pharmacotherapy for ketoacidosis. In the outpatient setting, pharmacists can educate patients on prevention of ketoacidosis and when to seek medical attention. Metabolic acidosis occurs as a result of increased endogenous acid production, a decrease in bicarbonate, or a buildup of endogenous acids.1 Ketoacidosis is a metabolic disorder in which regulation of ketones is disrupted, leading to excess secretion, accumulation, and ultimately a decrease in the blood pH.2 Acidosis is defined by a serum pH <7.35, while a pH <6.8 is considered incompatible with life.1,3 Ketone formation occurs by breakdown of fatty acids. Insulin inhibits beta-oxidation of fatty acids; thus, low levels of insulin accelerate ketone formation, which can be seen in patients with diabetes. Extr Continue reading >>

Index Of Suspicioncase 1: Acute, Intermittent, And Colicky Abdominal Pain In A 12-year-old Boycase 2: Emesis Since Birth In A 2½-month-old Infantcase 3: Worsening Cough Since Birth In A 16-month-old Toddler

Index Of Suspicioncase 1: Acute, Intermittent, And Colicky Abdominal Pain In A 12-year-old Boycase 2: Emesis Since Birth In A 2½-month-old Infantcase 3: Worsening Cough Since Birth In A 16-month-old Toddler

Case 1 Presentation A 12-year-old boy presents to the emergency department with acute-onset, intermittent, colicky right lower quadrant abdominal pain for 3 to 4 hours. The pain is associated with nausea and one episode of nonbilious, nonbloody vomiting. He has not had diarrhea, constipation, fever, urinary symptoms, trauma, or past similar episodes. On examination, the boy’s temperature is 38.8°C, his heart rate is 146 beats per minute, his respiratory rate is 26 breaths per minute, and his blood pressure is 110/65 mm Hg. He looks tired. His weight is 38.8 kg (35th percentile). Abdominal examination reveals a soft and nondistended abdomen, but he is tender in the left and right lower quadrants. He has no rebound tenderness, guarding, palpable masses, or organomegaly. The findings on the rest of the physical examination are unremarkable. Initial laboratory evaluations show hemoglobin of 13.6 g/dL, a white blood cell count of 18 × 103/μL (82% neutrophils, 12% lymphocytes, 6% monocytes, and 1% eosinophils), and a platelet count of 277 × 103/μL. His blood levels are as follows: total serum bilirubin, 0.6 mg/dL; direct bilirubin, <0.1 mg/dL; alanine aminotransferase, 18 IU/L; aspartate aminotransferase, 28 IU/L; alkaline phosphatase, 175 IU/L; amylase, 34 IU/L; and lipase, 42 IU/L. Serum electrolyte levels are normal. The only abnormality on urinalysis is 1+ blood. Abdominal radiographs show a nonspecific bowel gas pattern. Ultrasonography of the abdomen reveals elongated tubular structures with hypoechoic centers in the small intestine, which suggest a diagnosis (Fig 1). An additional study confirms the diagnosis. Download figure Open in new tab Download powerpoint Case 2 Presentation A 2-month-old boy is referred to our hospitalist service from an outside hospital. Continue reading >>

Acidosis: The Kiss Of Death!

Acidosis: The Kiss Of Death!

WHAT CAUSES A CONDITION CALLED "ACIDOSIS"? WHAT IS ACIDOSIS? Acidosis Definition: Acidosis is an increased acidity in the blood and other body tissue. Acidosis is said to occur when arterial pH falls below 7.35. The pH level of our blood affects every cell in our body. Chronic acidosis corrodes body tissue, and if left unchecked, will interrupt all cellular activities and functions. WHAT CAUSES ACIDOSIS? HIGH ACID-FORMING FOODS and DIETS all lead to ACIDOSIS. Living a fast-paced daily lifestyle, such as eating on the run and excessive over stimulation, will lead people to face a constant symptoms of indigestion and growing endangerment of over-acidification (Acidosis) of the body cells, which will interrupt cellular activities and functions. It is a major root of sickness and disease. Having our cells constantly exposed to an acidic environment leads to acidosis and then chronic acidosis and finally various forms of disease such as cancer and many more! Studies have shown that an acidic, anaerobic (which is also the lack of oxygen) body environment encourages the breeding of fungus, mold, bacteria, and viruses. As a result, our inner biological terrain shifts from a healthy oxygenated, alkaline environment to an unhealthy acidic one (acidic pH scale). This forces the body to constantly deplete its cellular energy to neutralize and detoxify these acids before they can act as poisons in and around the cells, ultimately changing the environment of each cell and finally compromising its immune system leaving it vulnerable to the ravages of disease to take a foothold in the body. When our body pH becomes overly acidic, it starts to set up defense mechanisms to keep the damaging acids from entering the vital organs. Modern Day Athletes and Acid-Forming Foods Unfortunately, Mo Continue reading >>

Exam Shows Diffuse Abdominal Tenderness With Guarding.

Exam Shows Diffuse Abdominal Tenderness With Guarding.

A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. 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. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>

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