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Dka Hypokalemia Or Hyperkalemia

Diagnosis And Treatment Of Diabetic Ketoacidosis (dka) In Dogs And Cats

Diagnosis And Treatment Of Diabetic Ketoacidosis (dka) In Dogs And Cats

What is DKA in Dogs and Cats? Diabetic Ketoacidosis (DKA) is a serious and life-threatening complication of diabetes mellitus that can occur in dogs and cats. DKA is characterized by hyperglycemia, ketonemia, +/- ketonuria, and metabolic acidosis. Ketone bodies are formed by lipolysis (breakdown) of fat and beta-oxidation when the metabolic demands of the cells are not met by the limited intracellular glucose concentrations. This provides alternative energy sources for cells, which are most important for the brain. The three ketones that are formed include beta-hydroxybutyrate, acetoacetate and acetone. Beta-hydroxybutyrate (BHB) and acetoacetate are anions of moderately strong acids contributing most to the academia (low blood pH). Acetone is the ketone body that can be detected on breath. In a normal animal, glucose enters the cell (with help of insulin) – undergoes glycolysis to pyruvate within cytosol – pyruvate moves into mitochondria (energy generating organelle in the cell) to enter the TCA cycle and ATP is formed. ATP is the main energy source of the body. When glucose cannot enter the cell, free fatty acids are broken down (lipolysis) and move into the cell to undergo beta-oxidation (creation of pyruvate). The pyruvate then moves into the mitochondria to enter the TCA cycle (by conversion to Acetyl-CoA first). However, when the TCA cycle is overwhelmed, the Acetyl-CoA is used in ketogenesis to form ketone bodies. Summary Diabetic Ketoacidosis (DKA) in Dogs and Cats When there is no insulin the body cannot utilize glucose and there is no intracellular glucose. The body then uses ketone bodes as an alternate source. When there is decreased insulin and increased counterregulatory hormones fatty acids are converted to AcCoA and then ketones. In the non-diabetic Continue reading >>

Hyperkalemia In Diabetic Ketoacidosis.

Hyperkalemia In Diabetic Ketoacidosis.

Abstract Patients with diabetic ketoacidosis tend to have somewhat elevated serum K+ concentrations despite decreased body K+ content. The hyperkalemia was previously attributed mainly to acidemia. However, recent studies have suggested that "organic acidemias" (such as that produced by infusing beta-hydroxybutyric acid) may not cause hyperkalemia. To learn which, if any, routinely measured biochemical indices might correlate with the finding of hyperkalemia in diabetic ketoacidosis, we analyzed the initial pre-treatment values in 131 episodes in 91 patients. Serum K+ correlated independently and significantly (p less than 0.001) with blood pH (r = -0.39), serum urea N (r = 0.38) and the anion gap (r = 0.41). The mean serum K+ among the men was 5.55 mmol/l, significantly higher than among the women, 5.09 mmol/l (p less than 0.005). Twelve of the 16 patients with serum K+ greater than or equal to 6.5 mmol/l were men, as were all eight patients with serum K+ greater than or equal to 7.0 mmol/l. Those differences paralleled a significantly higher mean serum urea N concentration among the men (15.1 mmol/l) than the women (11.2 mmol/l, p less than 0.01). The greater tendency to hyperkalemia among the men in this series may have been due partly to their greater renal dysfunction during the acute illness. However, other factors that were not assessed, such as cell K+ release associated with protein catabolism, and insulin deficiency per se, may also have affected serum K+ in these patients. 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 >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Definition: A hyperglycemic, acidotic state caused by insulin deficiency. The disease state consists of 3 parameters: Hyperglycemia (glucose > 250 mg/dl) Acidosis Ketosis Epidemiology Incidence of ~ 10,000 cases/year in US Mortality rate: 2-5% (prior to insulin was 100%) (Lebovitz 1995) Pathophysiology Insulin deficiency leads to serum glucose rise Increased glucose load in kidney leads to increased glucose in urine and osmotic diuresis Osmotic diuresis is accompanied by loss of electrolytes including sodium, magnesium, calcium and potassium Volume depletion leads to impaired glomerular filtration rate (GFR) Inability to properly metabolize glucose results in fatty acid breakdown with resultant ketone bodies (acetoacetate + beta-hydroxybutyrate) Causes: An acute insult leads to decompensation of a chronic disease. Can also be first manifestation of new onset diabetes (particularly in children). Below are common triggers Infection (particularly sepsis) Myocardial ischemia or infarction Medication non-compliance Clinical Presentation History Polydipsia, polyuria, polyphagia Weakness Weight loss Nausea/Vomiting Abdominal Pain Physical Examination Acetone odor on breath (“fruity” smell) Kussmaul’s respirations – deep fast breathing (tachypnea and hyperpnea) Tachycardia Hypotension Altered mental status Abdominal tenderness Diagnostic Testing Definitive diagnosis is established by laboratory criteria as detailed above (hyperglycemia, ketosis and acidosis) Essential Diagnostic Tests Serum glucose Typically > 350 mg/dL Euglycemic DKA (< 300 mg/dL) reported in up to 18% of patients Blood gas Patients will exhibit an anion gap metabolic Electrolytes: hypo/hyper/normokalemia, hyponatremia Arterial or venous blood gas can be used (Savage 2011) Urinalysis Glucosuria Ketonur Continue reading >>

Potassium Phosphate

Potassium Phosphate

Phosphorus Supplementation Similar to potassium, phosphate is deficient in animals with DKA regardless of the serum phosphorus concentration. Phosphorus is lost in patients with DKA because of a shift from the intracellular to the extracellular compartment secondary to hyperosmolality that is followed by urinary loss, decreased cellular uptake caused by insulin deficiency, inhibition of renal tubular phosphate absorption caused by acidosis, and osmotic diuresis.33,43 During treatment of DKA, the reduction in osmolality and insulin administration result in translocation of phosphate into the cell from the extracellular compartment. This translocation frequently causes a marked decrease in the plasma phosphorus concentration. However, clinically important consequences of hypophosphatemia are noted only when the serum phosphorus concentration is less than 1.0 to 1.5 mg/dL, and these signs are observed inconsistently. Hemolysis, muscle weakness, seizures, depression, and decreased leukocyte and platelet function leading to infection and bleeding can result from hypophosphatemia. The only abnormalities documented as caused by hypophosphatemia in veterinary DKA patients are hemolytic anemia in cats and possibly stupor and seizures in a dog.1,15,77 Hemolysis can occur despite phosphate supplementation and may have causes other than hypophosphatemia including oxidative injury.15,19 Hypophosphatemia is present at initial evaluation in 13% to 48% of cats and in 29% of dogs with DKA.15,20,37 Careful monitoring of serum phosphorus concentration during the initial 24 to 48 hours of management is important to identify severe hypophosphatemia necessitating phosphorus supplementation. Treatment of hypophosphatemia is indicated when the serum phosphorus concentration before treatment is Continue reading >>

On The Relationship Between Potassium And Acid-base Balance

On The Relationship Between Potassium And Acid-base Balance

The notion that acid-base and potassium homeostasis are linked is well known. Students of laboratory medicine will learn that in general acidemia (reduced blood pH) is associated with increased plasma potassium concentration (hyperkalemia), whilst alkalemia (increased blood pH) is associated with reduced plasma potassium concentration (hypokalemia). A frequently cited mechanism for these findings is that acidosis causes potassium to move from cells to extracellular fluid (plasma) in exchange for hydrogen ions, and alkalosis causes the reverse movement of potassium and hydrogen ions. As a recently published review makes clear, all the above may well be true, but it represents a gross oversimplification of the complex ways in which disorders of acid-base affect potassium metabolism and disorders of potassium affect acid-base balance. The review begins with an account of potassium homeostasis with particular detailed attention to the renal handling of potassium and regulation of potassium excretion in urine. This discussion includes detail of the many cellular mechanisms of potassium reabsorption and secretion throughout the renal tubule and collecting duct that ensure, despite significant variation in dietary intake, that plasma potassium remains within narrow, normal limits. There follows discussion of the ways in which acid-base disturbances affect these renal cellular mechanisms of potassium handling. For example, it is revealed that acidosis decreases potassium secretion in the distal renal tubule directly by effect on potassium secretory channels and indirectly by increasing ammonia production. The clinical consequences of the physiological relation between acid-base and potassium homeostasis are addressed under three headings: Hyperkalemia in Acidosis; Hypokalemia w Continue reading >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab 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

Hodaka Yamada1, Shunsuke Funazaki1, Masafumi Kakei1, Kazuo Hara1 and San-e Ishikawa2[1] Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan [2] Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Nasushiobara, Japan Summary Diabetic ketoacidosis (DKA) is a critical complication of type 1 diabetes associated with water and electrolyte disorders. Here, we report a case of DKA with extreme hyperkalemia (9.0 mEq/L) in a patient with type 1 diabetes on hemodialysis. He had a left frontal cerebral infarction resulting in inability to manage his continuous subcutaneous insulin infusion pump. Electrocardiography showed typical changes of hyperkalemia, including absent P waves, prolonged QRS interval and tented T waves. There was no evidence of total body water deficit. After starting insulin and rapid hemodialysis, the serum potassium level was normalized. Although DKA may present with hypokalemia, rapid hemodialysis may be necessary to resolve severe hyperkalemia in a patient with renal failure. Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment. Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria. Absolute insulin deficit alters potassium distribution between the intracellular and extracellular space, and anuria abolishes urinary excretion of potassium. Rapid hemodialysis along with intensive insulin therapy can improve hyperkalemia, while fluid infusions may worsen heart failure in patients with ketoacidosis who routinely require hemodialysis. Background Diabetic ketoacidosis (DKA) is a very common endocrinology emergency. It is usually associated with severe circulatory Continue reading >>

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Lack of insulin, thus no proper metabolism of glucose, ketones form, pH goes down, H+ concentration rises, our body tries to compensate by exchanging K+ from inside the cells for H+ outside the cells, hoping to lower H+ concentration, but at the same time elevating serum potassium. Most people are seriously dehydrated, so are in acute kidney failure, thus the kidneys aren’t able to excrete the excess of potassium from the blood, compounding the problem. On the other hand, many in reality are severely potassium depleted, so once lots of fluid so rehydration and a little insulin is administered serum potassium will plummet, so needs to be monitored 2 hourly - along with glucose, sodium and kidney function - to prevent severe hypokalemia causing fatal arrhythmias, like we experienced decades ago when this wasn’t so well understood yet. In practice, once the patient started peeing again, we started adding potassium chloride to our infusion fluids, the surplus potassium would be peed out by our kidneys so no risk for hyperkalemia. Continue reading >>

Esrd And Dka

Esrd And Dka

1. Thomas Lanning MD. Abdul Hamid Alraiyes MD. 2. 47 years old AAM Chief Complaints Nausea Vomiting Abdominal Pain CP 3. Past surgical Hx: Lt AKA (1 year ago) Rt AVF (radial artery) Rt Big toe amputation Lt IJ Dialysis catheter (3/10/2007) 4. Allergies: Penicillin “rash” Social History: Resident at Cleveland Rehab Denies any Hx of:  ETOH  Drug abuse  Ex- SMOKER Family History: DM HTN 5. Medications: Insulin aspart 5 units S.Q. Q AC Lantus 20 units S.Q. QHS Hydralazine 100mg P.O. Q8hr Lisinopril 20mg P.O. QD Lopressor 50mg P.O. BID Norvasc 10mg P.O. QD Renagel 800mg P.O. TID Nephrocap 1 tab P.O. QD Neurontin 300mg P.O. Q 8hr Fluoxetine 20mg P.O. QD Vancomycin 600mg I.V. with HD 6. Physical Exam:  V/S : 36- 120/56 - 62 – 17 - SPO2= 86% on RA  Pt is drowsy, dehydrated, not in distress  Skin: dry  Chest: Bil crackles, no wheezing + decreased air entry.  CVS: S1 + S2 + no M  ABD: soft, distended epigastric, tenderness, no rebound, BS+.  EXT: no edema , Lt AKA, Rt Big toe amputation, AVF on the Lt arm 7. Labs:  WBC = 10.9 , Hb= 12.6, Ht= 39.2, Plt= 184  Na= 119, K= 8, Cl= 86, CO2= 12 BUN= 103, Cr= 9.9 , Glucose=1140 8. Labs:  AG= 21 Serum Osmolality= 348 (275-290)  ABG= 7.048 / 41.8 / 75.1 / 11 A-a= 32 SAT= 86 FiO2 = 21% 9. 119 – (86 + 12) = 21 10. Expected AG = 21 + [ 2.5 X (4.5 – 3.8] = 22.75 11. PCO2 = (1.5 X 12 ) + 8 +/_ 2 = 28 - 24 12. PCO2 = (1.5 X 12 ) + 8 +/_ 2 = 28 – 24 ABG= 7.048 / 41.8 / 75.1 / 11 Metabolic Acidosis + Respiratory Acidosis 13. AG Excess / HCO3 deficit = 22 – 12 / 24 – 12 =~ 1 14. Labs:  Amylase= 102 Lipase=1082 LFT WNL ALP=242 CPP = 94 / 3 / 0.14 UA not done “Pt is anuric Continue reading >>

Hypokalemia And Hyperkalemia

Hypokalemia And Hyperkalemia

Sort Adrenal causes of hyperkalemia? Adrenal gland is important in secreting hormones such as cortisol and aldosterone. Aldosterone causes the kidneys to retain sodium and fluid while excreting potassium in the urine. Therefore diseases of the adrenal gland, such as Addison's disease, that lead to decreased aldosterone secretion can decrease kidney excretion of potassium, resulting in body retention of potassium, and hence hyperkalemia. How trauma leads to hyperkalemia Another cause of hyperkalemia is tissue destruction, dying cells release potassium into the blood circulation. Examples of tissue destruction causing hyperkalemia include: trauma, burns, surgery, hemolysis (disintegration of red blood cells), massive lysis of tumor cells, and rhabdomyolysis (a condition involving destruction of muscle cells that is sometimes associated with muscle injury, alcoholism, or drug abuse). What is role of potassium binders (Sodium polystyrene suffocate: SPS) SPS exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, decreasing the total body potassium level by approximately 0.5-1 mEq/L. Multiple doses are usually necessary. Onset of action ranges from 2 to 24 hours after oral administration and is even longer after rectal administration. The duration of action is 4-6 hours. Do not use SPS as a first-line therapy for severe life-threatening hyperkalemia; use it in the second stage of therapy. Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

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

Diabetic Ketoacidosis: Is There Hypokalemia?

Diabetic Ketoacidosis: Is There Hypokalemia?

This patient presented with diabetic ketoacidosis. The physicians were reluctant to start insulin until they knew that the potassium was not too low. They had difficult IV access. This EKG was recorded: There is sinus rhythm and a normal QRS. But repolarization is abnormal: there is scooped ST depression in I and aVL; there is a very prolonged QT interval (I measure a QT of 440 ms and QTc of 580 ms, though the computer got it very wrong at 440 ms); there are prominent U-waves (the bump between the T-wave and p-wave) in V2-V5. The ECG is pathognomonic of hypokalemia. When the level returned, it was 2.3 mEq/L. In a derivation study (which we have submitted only as an abstract so far) of ECGs of patients with hypokalemia vs. controls, in which interpreters were blinded to the K, we found very high sensitivity and specificity for a K less than vs. greater than 3.0 with any one of QTc of 450 ms or prominent U-waves or a subjective reading of hypokalemia. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Complication of type I diabetes result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis undiagnosed DM Presentation Symptoms abdominal pain vomiting Physical exam Kussmaul respiration increased tidal volume and rate as a result of metabolic acidosis fruity, acetone odor severe hypovolemia coma Evaluation Serology blood glucose levels > 250 mg/dL due to ↑ gluconeogenesis and glycogenolysis arterial pH < 7.3 ↑ anion gap due to ketoacidosis, lactic acidosis ↓ HCO3- consumed in an attempt to buffer the increased acid hyponatremia dilutional hyponatremia glucose acts as an osmotic agent and draws water from ICF to ECF hyperkalemia acidosis results in ICF/ECF exchange of H+ for K+ moderate ketonuria and ketonemia due to ↑ lipolysis β-hydroxybutyrate > acetoacetate β-hydroxybutyrate not detected with normal ketone body tests hypertriglyceridemia due to ↓ in capillary lipoprotein lipase activity activated by insulin leukocytosis due to stress-induced cortisol release H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted Treatment Fluids Insulin with glucose must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ be Continue reading >>

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