Abdominal Pain In Patients With Hyperglycemic Crises.
Abstract BACKGROUND: The aim of the study was to evaluate the incidence and prognosis of abdominal pain in patients with diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic state (HHS). Abdominal pain, sometimes mimicking an acute abdomen, is a frequent manifestation in patients with DKA. The prevalence and clinical significance of gastrointestinal symptoms including abdominal pain in HHS have not been prospectively evaluated. MATERIALS AND METHODS: This is a prospectively collected evaluation of 200 consecutive patients with hyperglycemic crises admitted to a large inner-city teaching hospital in Atlanta, GA.We analyzed the admission clinical characteristics, laboratory studies, and hospital course of 189 consecutive episodes of DKA and 11 cases of HHS during a 13-month period starting in October 1995. RESULTS: Abdominal pain occurred in 86 of 189 patients with DKA (46%). In 30 patients, the cause of abdominal pain was considered to be secondary to the precipitating cause of metabolic decompensation. Five of them required surgical intervention including 1 patient with Fournier's necrotizing fasciitis, 1 with cholecystitis, 1 with acute appendicitis, and 2 patients with perineal abscess. The presence of abdominal pain was not related to the severity of hyperglycemia or dehydration; however, a strong association was observed between abdominal pain and metabolic acidosis. In DKA patients with abdominal pain, the mean serum bicarbonate (9 +/- 1 mmol/L) and blood pH (7.12 +/- 0.02) were lower than in patients without pain (15 +/- 1 mmol/L and 7.24 +/- 0.09, respectively, both P <.001). Abdominal pain was present in 86% of patients with serum bicarbonate less than 5 mmol/L, in 66% of patients with levels of 5 to less than 10 mmol/L, in 36% of patients with Continue reading >>
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 >>
Metformin-associated Lactic Acidosis
OVERVIEW metformin use is associated with lactic acidosis, but it remians controversial as a disease entity MECHANISM the mechanism of lactic acidosis is uncertain Metabolic effects of metformin include: decreased gluconeogenesis increased peripheral glucose uptake decreased fatty acid oxidation CLINICAL FEATURES presence of risk factors abdominal pain nausea and vomiting fatigue myalgias altered mental status myocardial insufficiency multi-organ failure RISK FACTORS advanced age high dose renal failure (metformin is excreted unchanged in the urine) hypoxia active alcohol intake sepsis dehydration shock acidosis INVESTIGATIONS high anion gap metabolic acidosis (HAGMA) high lactate MANAGEMENT rule out other causes of lactic acidosis (sepsis, cardiogenic shock, hypoperfusion, ischaemic bowel) withdrawal of metformin RRT RRT remove metformin and correct acidosis best performed early due to large volume of distribution of metformin use hemodialysis use HCO3 buffer CONTROVERSY Some argue that metformin itself does not cause lactic acidosis, that it is actually due to the underlying conditions such as renal failure and diabetes mellitus. However, there are definite cases of lactic acidosis from acute metformin overdose with no other underlying risk factors. References and Links Journal articles Orban JC, Fontaine E, Ichai C. Metformin overdose: time to move on. Crit Care. 2012 Oct 25;16(5):164. [Epub ahead of print] PubMed PMID: 23110819; PubMed Central PMCID: PMC3682282. Salpeter SR, Greyber E, Pasternak GA, Salpeter EE. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010 Apr 14;(4):CD002967. doi: 10.1002/14651858.CD002967.pub4. Review. PubMed PMID: 20393934. FOAM and web resources Continue reading >>
Metabolic Acidosis
Vikipedi tasarımı üzerinden görüntüle. 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 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 ac Continue reading >>
Metabolic Acidosis: Causes, Symptoms, Diagnosis, Treatment, Prognosis, Prevention
Acidosis- A medical condition in which the fluids present in the body start to develop increased amount of acidic content making the body fluids acidic. There are two types of Acidosis- Respiratory Acidosis and Metabolic Acidosis. Respiratory Acidosis occurs as a result of malfunction of lungs. Metabolic Acidosis occurs as a result of malfunction of the kidneys. In this article, we will look into about Metabolic Acidosis. We will look into the causes, diagnosis, and treatment of Metabolic Acidosis. As stated, Metabolic Acidosis is a medical disorder in which the body starts producing excessive amounts of acid and/or the kidneys are not able to remove enough acidic content from the body. If not corrected at the appropriate time, Metabolic Acidosis can lead to a medical condition called acidemia in which pH scale in the blood gets low as a result of the kidneys being unable to form bicarbonates in the body. Causes Of Metabolic Acidosis The amount of acid in the blood can is determined by measuring the pH. A lower value of the pH means that the blood is acidic and a higher value of pH means that rhe blood is basic. Ideal pH value in the blood should be around 7.5. There are many processes in an individual's body which produces acid. Usually, the lungs and the kidneys take care of the excess production of acid; however, if there is a malfunction of these organs it results in Acidosis. As stated, Metabolic Acidosis begins in the kidneys. It develops when the kidneys are not able to discard excessive acid or in cases when they discard too much basic content from the body. Metabolic Acidosis is of three types: Diabetic Acidosis: This occurs in poorly controlled diabetes patients. In this form, there is formation of excess ketones making the blood acidic. Hyperchloremic Acidosi Continue reading >>
Acid-base Physiology
Case 15 : An old man with abdominal pain and shock Clinical Details An 85 year old man was admitted with severe abdominal pain and shock. The abdominal pain had started about 1500hrs and quickly became quite severe. There was no radiation to the back. The patient was known to have an abdominal aortic aneurysm (AAA). On arrival at hospital, the patient was shocked with peripheral circulatory failure and hypotension (BP 70-80 systolic). His abdomen was guarded and quite tender. He was distressed but able to talk and could understand instructions. Past history was of hypertension (on metoprolol and prazosin) and angina (on Isordil). Prior to this event, the patient was mobile and independent. A ruptured AAA was diagnosed clinically and he was transferred to theatre for emergency laparotomy. On arrival in theatre, BP was 120 systolic. The patient was talking but distressed by pain with rapid respirations at a rate of 30/min. It was noted that neck veins were very distended. An external jugular triple lumen central line and a brachial arterial line were placed before the surgical team had arrived in theatre. CVP was +40 mmHg. The blood gases were collected from an arterial line during preoxygenation with 100% oxygen at 1738 hrs (i.e. about 4.5 hours after onset of symptoms). Investigations: Biochemistry at 1520hrs was Na+ 138, K+ 4.9, Cl- 107, Bicarbonate 20, Glucose 11.2, Urea 12.8, creatinine 0.188, lactate 8.3 (all results in mmol/l). Haemoglobin 133 G/l. pH 7.35 pCO2 24 mmHg pO2 182 mmHg HCO3 13.8 mmol/l Assessment Initial clinical assessment The clinical expectation was an acute metabolic acidosis (lactic acidosis) due to peripheral circulatory failure, and respiratory alkalosis due to pain-induced hyperventilation. Respiratory compensation for the metabolic acidosis wo Continue reading >>
Diabetic Ketoacidosis
Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note 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 >>
Metabolic Acidosis
Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>
Lactic Acidosis And Pancreatitis
All nukes (d4T, ddI, abacavir, tenofovir, FTC, 3TC, AZT), hydroxyurea and ribavirin, have been linked to reports of lactic acidosis and/or pancreatitis. PIs and efavirenz have also been associated with pancreatitis. Lactic acidosis Lactic acidosis is a very serious side effect but it is no longer reported in countries that no longer use d4T, ddI and AZT. Although other nukes are linked to lactic acidosis one or more of these nukes are linked to most cases. Lactic acid is a by-product formed when the body breaks down starches and sugars. Levels of lactic acid are normally carefully regulated by the liver. Small increases in lactic acid (called hyperlactataemia) are relatively frequent, and are temporary, especially after exercise. If they reach a higher level, there is a risk of lactic acidosis. This is a potentially fatal side effect related to nucleoside/tide analogues. It is now rarely reported. Not only are nukes included in nearly all HIV combinations, but the symptoms of lactic acidosis are common side effects or symptoms. Symptoms Symptoms include: Unexplained tiredness, often severe Sickness (vomiting) and nausea Pain in the stomach, abdomen and/or liver Unexplained weight loss Difficulty breathing Poor blood circulation – cold hands or feet or bluish skin colour Sudden peripheral neuropathy Before combination therapy was available, this was only very rarely seen in HIV, and might well have been under diagnosed. Drug packaging now includes a clearer warning about this risk. Pregnancy might be an additional risk factor for lactic acidosis when using nukes. For this reason d4T or ddI are not recommended during pregnancy when alternative drugs are available. Lactic acidosis is diagnosed through examination, lab tests and an abdominal CT scan or liver biopsy. Altho Continue reading >>
Blood Gases And Acute Pancreatitis
Summarized from Sharma V, Devi T, Sharma R et al. Arterial pH, bicarbonate levels and base deficit at presentation as markers of predicting mortality in acute pancreatitis: a single-centre prospective study. Gastroenterol Rep (Oxf) 2014; 2(3): 226-31 Acute pancreatitis, i.e. acute inflammation of the pancreas, causes sudden onset of severe upper abdominal pain often radiating to the back. Other symptoms include vomiting, constipation and pyrexia. Two main causes - alcohol abuse and gall stone disease – account for the majority (~80 %) of cases. The condition has a variable course. In many cases inflammation resolves with little or no intervention over a period of a few days to a week, with no long-term consequences, but in others the condition can be severe, progressing rapidly to systemic inflammation, sepsis and multiple organ failure. Severe acute pancreatitis is thus a potentially fatal condition that warrants immediate admission to intensive care. A major problem for initial emergency room management of patients presenting with acute pancreatitis is to distinguish those whose course is likely to be benign from those who are likely to suffer severe disease and therefore require admission to intensive care. There is currently no single reliable prognostic test and clinicians must depend on rather cumbersome clinical scoring systems to predict outcome. The authors of a recently published study sought to examine the value of admission acid-base parameters (pH, bicarbonate and base excess) in predicting outcome among patients with acute pancreatitis. The notion that these might be useful prognostic markers is based partially on the observation that metabolic acidosis (characterized by reduced pH, bicarbonate and base excess) is a frequent complication of severe acute 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
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 >>
Abdominal Pain, Vomiting, And Confusion
In the latest Case Record of the Massachusetts General Hospital, a 54-year-old woman with type 2 diabetes mellitus was admitted to the hospital because of abdominal pain, vomiting, and confusion. Initial laboratory evaluation revealed a serum lactate level of 20.3 mmol per liter and a venous blood pH of 6.62. A diagnosis was made. Metformin is excreted unmetabolized in the urine. Therefore, impaired kidney function may result in the accumulation of metformin in the plasma, causing lactic acidosis. In patients who have toxic effects of metformin, the mechanism of lactic acidosis is multifactorial, including enhanced conversion of glucose to lactate in the small intestine and inhibition of gluconeogenesis by lactate, pyruvate, and alanine. Clinical Pearls Conditions that may cause a very large anion gap acidosis include lactic acidosis, aspirin overdose, methanol or ethylene glycol toxicity, diabetic ketoacidosis, and uremia. Altered mental status, including lethargy, stupor, and even coma, can be a direct consequence of acidosis. Acidemia may lead to increased vasodilatation and warm skin, and may also be associated with a paradoxical hypothermia, which is a known complication of profound acidosis. Cardiovascular consequences of acidosis include cardiac failure and catecholamine release, which may lead to arrhythmia and some degree of respiratory compromise. Acidemia can also cause gastric atony, nausea, vomiting, and abdominal pain. Morning Report Questions Q: What is a nonhypoxic (type B) lactic acidosis? A: Type B lactic acidosis refers to the impaired lactate metabolism that can occur in association with the administration of certain medications (e.g., metformin, salicylate, isoniazid, and zidovudine) or in association with certain cancers (e.g., lymphoma and leukemi Continue reading >>
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 >>
Chronic Metabolic Acidosis Destroys Pancreas
Peter Melamed and Felix Melamed Biotherapy Clinic of San Francisco, USA *Corresponding Author: Biotherapy Clinic of San Francisco 2215 Post Street, Suite 1, San Francisco, CA 94115, USA Phone 1 415 3776643 Fax 1 415 4093909 [email protected] Visit for more related articles at JOP. Journal of the Pancreas Abstract One primary reason for the current epidemic of digestive disorders might be chronic metabolic acidosis, which is extremely common in the modern population. Chronic metabolic acidosis primarily affects two alkaline digestive glands, the liver, and the pancreas, which produce alkaline bile and pancreatic juice with a large amount of bicarbonate. Even small acidic alterations in the bile and pancreatic juice pH can lead to serious biochemical/biomechanical changes. The pancreatic digestive enzymes require an alkaline milieu for proper function, and lowering the pH disables their activity. It can be the primary cause of indigestion. Acidification of the pancreatic juice decreases its antimicrobial activity, which can lead to intestinal dysbiosis. Lowering the pH of the pancreatic juice can cause premature activation of the proteases inside the pancreas with the potential development of pancreatitis.The acidification of bile causes precipitation of the bile acids, which irritate the entire biliary system and create bile stone formation. Aggressive mixture of the acidic bile and the pancreatic juice can cause erratic contractions of the duodenum’s walls and subsequent bile reflux into the stomach and the esophagus. Normal exocrine pancreatic function is the core of proper digestion. Currently, there is no effective and safe treatment for enhancing the exocrine pancreatic function. Restoring normal acid-base homeostasis can be a useful toolfor pathophysi Continue reading >>
Diabetic Ketoacidosis
Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>
