Pathogenesis, diagnosis and treatment of the acute complications of Diabetes Mellitus

Signs, symptoms, pre-disposing factors and features of the various kinds of acute diabetic complications

A predisposing factor of Non-ketonic hyperglycemia (hyperosmolar Coma)
A predisposing factor of Non-ketonic hyperglycemia (hyperosmolar Coma) | Source
A sign and symptome of Diabetes Ketoacidosis
A sign and symptome of Diabetes Ketoacidosis | Source
One of the things you observe during the physical examination of Lactic Acidosis
One of the things you observe during the physical examination of Lactic Acidosis | Source
A clear view
A clear view | Source
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma | Source
A predisposing factor of hypoxia
A predisposing factor of hypoxia | Source
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma | Source
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma | Source
MRI view of cerebral edema
MRI view of cerebral edema | Source
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma | Source
One of the major signs and symptoms of a patient with Diabetic keto-acidosis
One of the major signs and symptoms of a patient with Diabetic keto-acidosis | Source
A predisposing factor of Hypoxia
A predisposing factor of Hypoxia | Source
A predisposing factor of Diabetic Ketoacidosis
A predisposing factor of Diabetic Ketoacidosis | Source
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma | Source
A predisposing factor of Diabetic Ketoacidosis
A predisposing factor of Diabetic Ketoacidosis | Source
A predisposing factor of Diabetic Ketoacidosis
A predisposing factor of Diabetic Ketoacidosis | Source
One of the major signs and symptoms of a patient with Diabetic keto-acidosis
One of the major signs and symptoms of a patient with Diabetic keto-acidosis | Source
One of the major signs and symptoms of a patient with Diabetic keto-acidosis
One of the major signs and symptoms of a patient with Diabetic keto-acidosis | Source
A predisposing factor of Diabetic Ketoacidosis
A predisposing factor of Diabetic Ketoacidosis | Source
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma | Source
One of the major signs and symptoms of a patient with Diabetic keto-acidosis
One of the major signs and symptoms of a patient with Diabetic keto-acidosis | Source
A predisposing factor of Diabetic Ketoacidosis
A predisposing factor of Diabetic Ketoacidosis | Source
A predisposing factor of Diabetic Ketoacidosis
A predisposing factor of Diabetic Ketoacidosis | Source
One of the major signs and symptoms of a patient with Diabetic keto-acidosis
One of the major signs and symptoms of a patient with Diabetic keto-acidosis | Source
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma | Source
One of the major signs and symptoms of a patient with Diabetic keto-acidosis
One of the major signs and symptoms of a patient with Diabetic keto-acidosis | Source
It could be affected in Diabetes Keto-acidosis
It could be affected in Diabetes Keto-acidosis | Source
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma
A predisposing factor of Non-ketonic Hyperglycemic Hyperosmolar Coma | Source
A predisposing factor of Diabetic Ketoacidosis
A predisposing factor of Diabetic Ketoacidosis | Source
One of the major signs and symptoms of a patient with Diabetic keto-acidosis
One of the major signs and symptoms of a patient with Diabetic keto-acidosis | Source
One of the major signs and symptoms of a patient with Diabetic keto-acidosis
One of the major signs and symptoms of a patient with Diabetic keto-acidosis | Source

INTRODUCTION

Hello everyone and welcome to the second edition of disease cases been clinically analyzed and treated here in my internet hospital. Today's case would be on the acute complications of Diabetes mellitus closely following the first case we treated, which is Diabetes Mellitus itself. You may want to go through it first before reading this, it would be very great if you do so, but if you want to have a glance and a view of what diabetes is all about, I suggest, you go to this link and have a short glance to prepare your mind on what is to come from this hub

Diabetes Mellitus in simple plain language

Then come back here and read the detailed clinical explanations of the acute complications of Diabetes Mellitus. Most of the literals on the street just see diabetes as a simple illness involving an increased level of glucose in blood. In fact some see it as a sugar-related disease not even knowing what sugar is involved. But if will blow your mind to see how devastating, vast, broad and complicating diabetes is. If you'd followed us from the previous hub about diabetes, you will see the effects and long term complications of Diabetes which also includes sexual complications both to men and women. Diabetes is a disease worth knowing so that each and every one of us can apply adequate preventive measures in order not to acquire it. A link of my previous hub on diabetes will be shown at the end of this hub, so that you may read it if you please to.


Classification of acute complications of DM

1. Diabetic coma:

1) diabetic ketoacidisis (DKA);

2) nonketonic hyperglycemic-hyperosmolar coma (NKHHC);

3) lactoacidosis (LA).

2. Hypoglycemic coma (HC).

DIABETIC KETOACIDISIS (DKA)

DKA is the most frequent endocrine emergency seen by the primary care physician. Mortality rates from 6 – 10 % have been reported. All the abnormalities associated with DKA can be traced to an absolute or relative insulin lack, which develops over the period of several hours or days.

DKA results from grossly deficient insulin modulation of glucose and lipid metabolism.

Major components of the pathogenesis of diabetic ketoacidosis are reductions in effective concentrations of circulating insulin and concomitant elevations of counterregulatory hormones (catecholamines, glucagon, growth hormone and cortisol).

These hormonal alterations bring about three major metabolic events:

(1) hyperglycemia (high level of glucose in blood) resulting from accelerated gluconeogenesis ( the production of glucose by using new and different sources such as amino acids, fats etc) and decreased glucose utilization,

(2) increased proteolysis (the break down of proteins) and decreased protein synthesis (the production of proteins) and

(3) increased lipolysis (the breakdown of Lipids) and ketone production.

Hyperglycemia initially causes the movement of water out of cells, with subsequent intracellular dehydration, extracellular fluid expansion and hyponatremia (low level of sodium in blood). It also leads to a diuresis in which water losses exceed sodium chloride losses. Urinary losses then lead to progressive dehydration and volume depletion, which causes diminished urine flow and greater retention of glucose in plasma. The net result of all these alterations is hyperglycemia with metabolic acidosis and an increased plasma anion gap.

Precipitating factors:

1) newly diagnosed diabetes (presenting manifestation);

2) inadequate administration of exogenous insulin;

3) increased requirements for insulin caused by the presence of an underlying stressful condition:

- an intercurrent infection (pneumonia, cholecyctite);

- a vascular disorder (myocardial infarction, stroke);

- an endocrine disorder(hyperthyroidism, pheochromocytoma);

- trauma;

- pregnancy;

- surgery.

Factors Most Often Associated with the Development of Diabetic Ketoacidosis

Factor

Approximate frequency (%)

Infection: 35

Omission of insulin or inadequate insulin: 30

Initial presentation of diabetes mellitus: 20

Medical illness: 10

Unknown: 5

Clinical presentation

Diabetic ketosis

It is status which is characterized by increased level of ketones in blood, without clinical signs of dehydration and can be corrected by diet (fat restriction) and regular insulin injection.

DKA develops over a period of days or weeks.

Signs and symptoms

1. Polydipsia (Increased appetite), polyurea (increased and frequent Urination) and weakness are the most common presenting complaints.

2. Anorexia (eating disorder), nausea (Sensation of unease and discomfort in the upper stomach with an urge to vomit), vomiting, and abdominal pain may be present and mimic an abdominal emergency.

3. Ileus and gastric dilatation may occur and predispose to aspiration.

4. Kussmaul breathing (deep, sighing respiration) is present as respiratory compensation for the metabolic acidosis and is obvious when the pH is less than 7.2.

5. Symptoms of central-nervous-system involvement include headaches, drowsiness, lassitude, stupor and coma (only 10 % patients are unconscious).

Physical examination

1. Hypotermia is common in DKA. A fever should be taken as strong evidence of infection.

2. Hyperpnea or Kussmaul respiration are present and related to degree of acidosis, acetone may be detected on the breath (musty (fruity) odor to the breath).

3. Tachycardia (Increased heart rate which exceeds the normal range) frequently is present, but blood pressure is usually normal unless profound dehydration is present.

4. Poor skin tugor (an abnormality in the skin’s ability to change shape and return to normal elasticity) may be prominent depending on the degree of hydration.

5. Hyporeflexia (associated with low serum potassium- a condition of below-normal or absent reflexes which can be tested for by using a reflex hammer) can be elicited.

6. Signs consistent with a “surgical abdomen” but which follow severe ketonemia (presence of Ketone bodies in blood) can confuse the clinical picture.

7. In extreme cases of DKA one can see hypotonia (a state of low muscle tone) stupor (the lack of critical cognitive function and level of consciousness where in a sufferer is almost entirely unresponsive and only responds to base stimuli such as pain), coma, in-coordination of ocular movements, field dilated pupils, and finally death.

8. Other signs from a precipitating illness can be present.

Although usually straightforward, the diagnosis of diabetic ketoacidosis is occasionally missed in unusual situations, such as when it is the initial presentation of diabetes in infants or elderly patients or when patients present with sepsis or infarction of the brain, bowel or myocardium. These presentations can distract the physician from the underlying diagnosis of diabetic ketoacidosis.

The laboratory tests needed to confirm the presence of diabetic ketoacidosis and to screen for precipitating events.

Laboratory findings

1. The hallmark of DKA is the finding of:

- hyperglycemia;

- ketonemia;

- metabolic acidosis (plasma pH and bicarbonates are decreased.

2. A presumptive bedside diagnosis is justified if the urine is strongly positive for both glucose and ketones.

3. Different changes of electrolyte levels in the blood can be observed and does not reflect the actual total body deficits.

4. Serum amylase and transaminases can be elevated.

5. Leucocytosis (Production of white blood cells) occurs frequently in DKA and therefore cannot be used as a sole indication of infectious process.

Types of DKA:

- abdominal;

- vascular collapse;

- cerebral (encephalopathic);

- renal;

- mixed.

Treatment

The management of patients may be difficult because of problems in achieving of normal glucose control. Because there is good evidence that hyperglycemia conveys risks for all of the common long-term complications of DM, which are the major cases of excess morbidity and mortality in diabetics.

Patients with type 1 DM usually start treatment at the hospital. They require close monitoring during efforts to develop an appropriate insulin treatment regimen, and the patients or their care givers require detailed education in their responsibilities and proficiency in them before home management is safe.

Most patients with type 2 DM who are not acutely ill can be safety started on the insulin (if they need it) on an outpatient basis with adequate patient education and close physician follow-up.

An effort to maintain persistently normal serum glucose fluctuations in diabetics entail significant risk of causing frequent or severe hypoglycemic episodes, particularly in type 1 DM patients. Treatment regimens differ in the priorities assigned to keeping the risks for hypoglycemia minimal and to keeping serum glucose fluctuations in a normal to near-normal range.

The therapeutic goals for diabetic ketoacidosis consist of improving circulatory volume and tissue perfusion, reducing blood glucose and serum osmolality toward normal levels, clearing ketones from serum and urine at a steady rate, correcting electrolyte imbalances and identifying precipitating factors.

The goals of therapy include:

1. Rehydratation.

2. Reduction of hyperglycemia.

3. Correction of: a) acid-base and b) electrolyte imbalance.

4. Investigation of precipitating factors, treatment of complications.

The most important factor to emphasize is the frequent monitoring of the patient both clinically and chemically. Initially, laboratory data should be obtained every 1 – 3 hours and less frequently once clinical improvement is noted. If the patient is in shock, stupor or coma, a nasogastric tube, especially if vomiting, and urinary catheter are recommended.

Frequent assessment of potassium status is vital. A lead II electrocardiogram (ECG) can be provide a rapid assessment of hyperkalemia (peaked T waves) and hypokalemia (flat T waves and presence of U waves). Hyporeflexia and ileus are clinical indications of potassium deficiency.

Careful observation of neurological status is vital to detect the infrequent but devastating presence of cerebral edema.

Rehydration(Fluid Replacement)

The severity of fluid and sodium deficits is determined primarily by the duration of hyperglycemia, the level of renal function and the patient's fluid intake.

The average fluid deficit in adults with DKA is 3 to 5 l.

Dehydration can be estimated by clinical examination and by calculating total serum osmolality and the corrected serum sodium concentration.

A rapid infusion of 0,9 % sodium chloride (e.g., 1 l/h for the first 1 to 2 hours) is given and then reduced to about 0,5 – 0,3 l/h if the blood pressure is stable and the urine follow is adequate. After the initial infusion, intravenous fluid therapy must be adjusted individually on the basis of urine output, clinical assessments of hydration and circulation, determination of plasma electrolytes and glucose. When serum glucose level is about 11 – 13 mmoll/ (approximately 250 mg per dL )l administration of 5 % glucose with insulin can be performed (1 to 2 unites of insulin on each 100 ml of 5 % glucose solution). The addition of glucose to the intravenous solution is necessary for correction of tissue lipolysis and acidosis. This allows continued insulin administration until ketonemia is controlled and also helps to avoid iatrogenic hypoglycemia.

Another important aspect of rehydration therapy in patients with diabetic ketoacidosis is the replacement of ongoing urinary losses.

Insulin treatment

Modern management of diabetic ketoacidosis has emphasized the use of lower doses of insulin.

This has been shown to be the most efficacious treatment in both children and adults with diabetic ketoacidosis. The current recommendation is to give low-dose (short-acting regular) insulin after the diagnosis of diabetic ketoacidosis has been confirmed by laboratory tests and fluid replacement has been initiated.

It is prudent to withhold insulin therapy until the serum potassium concentration has been determined. In the rare patient who presents with hypokalemia, insulin therapy may worsen the hypokalemia and precipitate life-threatening cardiac arrhythmias.

E.g., initial intravenous administration of 10 to 20 units of regular insulin followed by continuous intravenous infusion of 0,1 unit/kg/hour in 0,9 % sodium chloride infusion. (50 units of insulin can be added to a 500 ml bottle of 0,9 % sodium chloride solution to give 1 insulin unite/10 ml of solution.)

In clinical situations in which continuous intravenous insulin cannot be administered, the recommended initial insulin dose is 0.3 unit per kg, with one half of the dose given as an intravenous bolus and the remainder given subcutaneously or intramuscularly Subsequently, regular insulin should be given in a dosage of 0.1 unit per kg per hour until the blood glucose level is approximately 11 – 13 mmoll/L (250 mg per dL).

If the blood glucose concentration does not fall by 2.8 to 3.9 mmol per L (50 to 70 mg per dL) in the first hour, the intravenous infusion rate should be doubled or additional intravenous 10-unit boluses of insulin should be given every hour Either of these treatments should be continued until the blood glucose level falls by 2.8 to 3.9 mmol per L (50 to 70 mg per dL) Low-dose insulin therapy typically produces a linear fall in the glucose concentration of 2.8 to 3.9 mmol per L (50 to 70 mg per dL).

More rapid correction of hyperglycemia should be avoided because it may increase the risk of cerebral edema. This dreaded treatment complication occurs in approximately 1 percent of children with diabetic ketoacidosis. The typical presentation is onset of headache and decreased mental status occurring several hours after the start of treatment. Cerebral edema is associated with a mortality rate of up to 70 percent.

But if there is a tendency for decreasing the level of glucose we have to decrease the dose of insulin in two times.

When the serum glucose concentration reaches 11-13 mmoll/l, hourly insulin dosage can be reduced to 0.05 unit per kg per hour or insulin can be given subcutaneously (if plasma and urine persistently negative for ketones). Blood glucose level should be maintained at about 11 mmoll/l during intravenous therapy.

Improvement usually is noted in 8 – 24 hours. Following stabilization of the clinical condition, patients are placed in insulin regimen consisting of five injections of regular insulin.

Treatment of electrolyte disorders.

As a rule, potassium should never be given until the state of renal function is known and until the serum potassium concentration is available.

Although the typical potassium deficit in diabetic ketoacidosis is 500 to 700 mEq (500 to 700 mmol), most patients are hyperkalemic at the time of diagnosis because of the effects of insulinopenia, hyperosmolality and acidemia. During rehydration and insulin therapies for diabetic ketoacidosis, the serum potassium concentration typically declines rapidly as potassium reenters the intracellular compartment.

The initiation of K replacement (20 to 40 mmoll/h) usually can be deferred for 2 hours, using hourly serum measurements as a guide.Potassium would be to infuse at a rate of ml of 1,5 g/h during 3 – 5 hours.

The goal is to maintain the serum potassium concentration in the range of 4 to 5 mEq per L (4 to 5 mmol per L).

Correction of metabolic acidosis.

The metabolic acidosis occurs due to insulin deficiency and dehydration. So ketone bodies are themselves metabolized to bicarbonate once proper therapy is begun (fluids, electrolytes, insulin) and exogenous administration of bicarbonate can overcorrect to alkalosis.

The use of bicarbonate can be recommended only in the following cases:

- if life-threatening hyperkalemia;

- when severe lactic acidosis complicates DKA;

- with severe acidosis (pH<7), especially when complicated by shock that is not responsive to appropriate fluid resuscitative measures in an attempt to improve cardiac output.

Bicarbonate would be to infuse at a rate of 100 to 300 ml of 2,5 % solution.

Other therapeutic consideration:

- since infection is one of the leading precipitating events of DKA, it should be looked for and, if found, treated appropriately;

- vascular thrombosis (it is secondary to severe dehydration, high serum viscosity, and low cardiac output) – heparin (5000 unites 4 times a day);

- vascular collapse can be treated by mesatone (1 – 2 ml); glucocorticoides (dexametasone 4 mg two times a day). You must remember that development of vascular collapse after initiation of therapy should suggest the presence of gram-negative sepsis or silent myocardial infarction;

- cerebral edema (It is a rare and frequently fatal complication. Some physicians believe that rapid osmotic reduction of plasma glucose should be avoided to minimize rapid osmotic changes. Some patients have premonitory symptoms (e.g., sudden headache, rapid decrease in the level of consciousness), but in others acute respiratory arrest is the initial manifestation. If cerebral edema is diagnosed, therapeutic maneuvers might include the use of : mannitol (1 – 2 g/kg intravenous over 20 min), dexametasone (0,25 – 0,50 mg/kg/day divided q 4 – 6 h). But they are usually ineffective after the onset of respiratory arrest.

Immediate Posthyperglycemic Care

In patients who are unable to eat, 5 percent dextrose in hypotonic saline solution is continued at a rate of 100 to 200 mL per hour. Blood glucose levels are monitored every four hours, and regular insulin is given subcutaneously every four hours using a sliding scale. When patients are able to eat, multidose subcutaneous therapy with both regular (short-acting) and intermediate-acting insulin may be given.

In patients with newly diagnosed diabetes, an initial total insulin dosage of 0.6 to 0.7 unit per kg per day is usually adequate to achieve metabolic control. A typical regimen is two thirds of the total daily dosage before breakfast and one third of the total daily dosage before dinner, with the insulin doses consisting of two-thirds NPH (intermediate-acting) insulin and one-third regular (short-acting) insulin.

Patients with known diabetes can typically be given the dosage they were receiving before the onset of diabetic ketoacidosis.

Complications of Therapy

Symptomatic cerebral edema occurs primarily in pediatric patients, particularly those with newly diagnosed diabetes. No single factor predictive for cerebral edema has yet been identified. As noted previously, however, overly rapid rehydration or overcorrection of hyperglycemia appears to increase the risk of cerebral edema. Onset of headache or mental status changes during therapy should lead to consideration of this complication. Intravenous mannitol in a dosage of 1 to 2 g per kg given over 15 minutes is the mainstay of therapy. Prompt involvement of a critical care specialist is prudent.

Adult respiratory distress syndrome (ARDS) is a rare but potentially fatal complication of the treatment of diabetic ketoacidosis. Excessive crystalloid infusion favors the development of pulmonary edema, even in the presence of normal cardiac function. Patients with an increased alveolar to arterial oxygen gradient (AaO2) and patients with pulmonary rales on physical examination may be at increased risk for ARDS. Monitoring of oxygen saturation with pulse oximetry may assist in the management of such patients.

Hyperchloremic metabolic acidosis with a normal anion gap typically persists after the resolution of ketonemia. This acidosis has no adverse clinical effects and is gradually corrected over the subsequent 24 to 48 hours by enhanced renal acid excretion. The severity of hyperchloremia can be aggravated by excessive chloride administration in hydration fluids.

NONKETONIC HYPERGLYCEMIC-HYPEROSMOLAR COMA (NKHHC OR HNC)

HNC is a syndrome characterized by impaired consciousness, sometimes accompanied by seizures, extreme dehydration, , and extreme hyperglycemia that is not accompanied by ketoacidosis.

The syndrome usually occurs in patients with type II DM, who are treated with a diet or oral hypoglycemic agents, sometimes it is a complication of previously undiagnosed or medically neglected DM (type II).

In contrast to ketoacidosis, mortality in patients with HNC has been very high (50 %) in most series. Mortality has been associated with convulsions, deep vein thrombosis, pulmonary embolus, pancreatitis and renal failure. Death is usually due to an associated severe medical condition and not to the hyperosmolality.

The pathophysiology of HNC is similar to that of ketoacidosis, except that ketoacids do not accumulate in the blood. The reason of this phenomenon is unclear. Initially it was thought that patients with HNC produced enough insulin to prevent lipolysis and ketogenesis but not enough to prevent hyperglycemia. The concept was invalidated by finding similar inappropriately low plasma insulin concentrations in patients with the two syndromes. The finding of lower plasma free fatty acids, as well as cortisol and growth-hormone concentrations, in patients with ketoacidosis has raised the possibility that the absence of ketosis may be the result of decreased cortisol and growth-hormone effects on lipolysis. Suppression of lipolysis by hyperosmolality also has been proposed.

HNC usually develops after a period of symptomatic hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration from the hyperglycemia-induced osmotic diuresis.

Predisposing factors.

1. HNC seems to occur spontaneously in about 5 – 7 % of patients.

2. In 90 % of patients some degree of renal insufficiency seems to coexist.

3. Infection (e.g., pneumonia, urinary tract infection, gram-negative sepsis) is underlying frequent precipitating cause.

4. Use of certain drugs has been associated with this condition:

- steroids increase glucogenesis and antagonize the action of insulin;

- potassium-wasting diuretics (hypokalemia decreases insulin secretion), e.g., thiazides, furosemide;

- other drugs, e.g., propranolol, azathioprine, diazoxide.

5. Other medical conditions such as cerebrovascular accident, subdural hematoma, acute pancreatitis, and severe burns have been associated with HNC.

6. Use of concentrated glucose solutions, such as used in peripheral hyperalimentation or renal dialysis, has been associated with HNC.

7. HNC can be induced by peritoneal or hemodialysis, tube feeding.

8. Endocrine disorders such as acromegaly, Cushing disease, and thyrotoxicosis have also been associated with HNC.

Clinical presentation

Signs and symptoms.

1. Polyuria, polydipsia, weight loss, weakness and progressive changes in state of consciousness from mental cloudiness to coma (present in 50 % of patients) occur over a number of days to weeks.

2. Because other underlying conditions (such as cerebrovascular accident and subdural hematoma) can coexist, other causes of coma should be kept in mind, especially in the elderly.

3. Seizures occur in 5 % of patients and may be either focal or generalized.

Physical examination.

1. Severe dehydration is invariably present.

2. Various neurologic deficits (such as coma, transient hemiparesis, hyperreflexia, and generalized areflexia- absence of neurologic reflexes such as the knee jerk reaction) are commonly present. Altered states of consciousness from lethargy ( a state of being lazy, sluggish, or indifferent) to coma are observed.

3. Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.

Laboratory findings.

1. Extreme hyperglycemia (blood glucose levels from 30 mmoll/l and over are common.

2. A markedly elevated serum osmolality is present, usually in excess of 350 mOsm/l. (Normal = 290 mOsm/l). The osmolality can be calculated by the following formula: mOsm/l = 2(Na + K) = blood glucose/18 + BUN/2.8.

3. The initial plasma bicarbonate averaged.

4. Serum ketones are usually not detectable, and patients are not acidic.

5. Serum sodium may be high (if severe degree of dehydration is present), normal, or high (when the marked shift of water from the intracellular to the extracellular space due to the marked hyperglycemia is present).

6. Serum potassium levels may be high (secondary to the effects of hyperosmolality as it draws potassium from the cells), normal, or low (from marked urinary losses from the osmotic diuresis). But potassium deficiency exists.

Treatment

This condition is a medical emergency and the patient should be placed in an intensive care unit.

Many of the management techniques recommended for a patient with DKA are applicable here as well.

The goals of therapy include:

- rehydration;

- reduction of hyperglycemia;

- electrolytes replacement;

- investigation of precipitating factors, treatment of complications.

Rehydration.

The average fluid deficit is 10 liters, and acute circulatory collapse is a common terminal event in HNC. The immediate aims of treatment are to rapidly expand the contracted intravascular volume in order to stabilize the blood pressure, improve the circulation, and improve the rate of urine production. It is important to remember that it is the severe hyperglycemia and the concomitant obligatory shift of water from the intracellular to the intravascular compartment that prevents this latter space from collapsing at the time of severe fluid depletion. With too rapid a correction of hyperglycemia, potential hypovolimic shock (as fluid moves from the extracellular space back into the intracellular space) may occur.

Treatment is starting by infusion 1 to 3 liters of 0,9 % sodium chloride over 1 to 2 hours; if this suffices to stabilize the blood pressure, circulation and restore good urine flow, the intravenous fluid can be changed to 0,45 % sodium chloride to provide some free water. 0,45 % sodium chloride is used at a rate of 150 to 500 ml/hour depending on the state of hydration, previous clinical response and the balance between fluid input and output. The aim of this phase of intravenous fluid therapy is not to attempt to rapidly correct the total fluid deficit or the hyperosmolality, but rather to maintain stable circulation and renal function and to progressively replenish water and sodium at rates that do not threaten or cause acute fluid overload.

Generally, half of the loss is replaced in the first 12 hours and the rest in the subsequent 24 hours.

Insulin therapy.

Insulin treatment in HNC is started by 10 to 20 unites of regular insulin intravenously as a bolus dose prior to starting the insulin infusion and then giving intravenously regular insulin in a dose of 0,05 – 0,10 unites/kg/hour (many authorities routinely use the same insulin treatment regimens as for treating DKA, other authorities recommend smaller doses of insulin, because they believe that patients with type II DM are offer very sensitive to insulin, but this view is not universally accepted, and many obese type II diabetics with NHC require larger insulin doses to induce a progressive decrease in their marked hyperglycemia. It is important to remember that because of insulin therapy causes blood glucose levels to fall, water shifts into the cells and existing hypotension and oliguria can further aggravated. Thus, initially some advocate delaying insulin therapy while infusion normal saline until vital signs have improved.

When the plasma glucose reaches the range 11 to 13 mmoll/l, 5 % glucose should be added to the intravenous fluids to avoid the risk of hypoglycemia. Following recovery the acute episode, patients are usually switched to adjusted doses of subcutaneous regular insulin at 4 to 6-hour intervals. When they are able to eat, this is changed to a 1 or 2 injection regimen.

Treatment of electrolyte disorders.

Once urine flow has been reestablished, potassium should be added to begin repletion of the total body deficits.

Potassium replacement is usually started by adding 20 mmoll/l to the initial liter of the intravenously-infused 0,45 % sodium chloride with careful serum potassium and ECG monitoring.


Contributors And acknowledgements

Professor of Nephrology. Department of internal medicine for foreign students, Ternopil state Medical university, Ukraine
Professor of Nephrology. Department of internal medicine for foreign students, Ternopil state Medical university, Ukraine | Source
Professor of Pharmacology, Pharmacology department, Ternopil state Medical University, Ukraine.
Professor of Pharmacology, Pharmacology department, Ternopil state Medical University, Ukraine. | Source
Pharmacology department, Ternopil state medical University, Ukraine.
Pharmacology department, Ternopil state medical University, Ukraine. | Source
Pharmacology department, Ternopil state medical University, Ukraine.
Pharmacology department, Ternopil state medical University, Ukraine. | Source
Pharmacology department, Ternopil state medical University, Ukraine.
Pharmacology department, Ternopil state medical University, Ukraine. | Source
Internal medicine department for foreign students, Ternopil state Medical University, Ukraine.
Internal medicine department for foreign students, Ternopil state Medical University, Ukraine. | Source
Biochemistry department, Ternopil state Medical University, Ukraine
Biochemistry department, Ternopil state Medical University, Ukraine | Source
Department of Internal Medicine for foreign students, Ternopil state Medical University, Ukraine
Department of Internal Medicine for foreign students, Ternopil state Medical University, Ukraine | Source
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LACTIC ACIDOSIS (LA)


DM is one of the major causes of LA, a serious condition characterized by excessive accumulation of lactic acid and metabolic acidosis.

Pyruvic acid Lactic acid

NADH NAD

Acetoacetic Beta-hydroxybutyric

The hallmark of LA is the presence of tissue hypoxemia (reduced concentration of oxygen in blood), which leads to enhanced anaerobic glycolysis and to increased lactic acid formation.

Pyruvic acid is converted into lactic acid by lactic dehydrogenase (LDH) in the presence of reduced nicotinamide adenine dinucleotide (NADH), which, in turn, is converted into NAD. The reaction is reversible and involves LDH in both directions. The conversion of acetoacetic acid into beta-hydroxybutyric acid also requires the oxidation of NADH. LA results from decreased availability of NAD caused by lack of oxygen. Likewise, the deficiency of NAD impairs the conversion of beta-hydroxybutyric into acetoacetic acid. Thus, LA predisposes to accumulation of beta-hydroxybutyric acid, which does not react with acetest tablet, so, the reaction for ketone bodies may be negative or slightly positive. The normal blood lactic acid concentration is 1mmol/l, and the pyruvic to lactic ratio is 10:1. An increase in lactic acid without concomitant rise in pyruvate leads to LA of clinical importance.

Predisposing factors

1. Heart and pulmonary failure (which leads to hypoxia).

2. Usage of biguanids, pheformin therapy.

3. Alcohol intoxication.

4. Ketoacidosis (it is important to have a very high index of suspection with respect to presence of LA).

Clinical presentation

Signs and symptoms.

1. Kussmaul breathing (deep, sighing respiration) is present as respiratory compensation for the metabolic acidosis and is obvious when the pH is less than 7.2.

2. Symptoms of central-nervous-system involvement include headaches, drowsiness, lassitude (weariness of body or mind from strain, oppression climate; exhaustion, lethargy etc).

3. Anorexia, nausea, vomiting, and abdominal pain may be present.

4. Myalgia (Muscle pain) is common.

Physical examination.

1. Acrocyanosis (perisistent blue or cyanotic discoloration of the digits, ost commonly seen in the hands, although also occurring in the face and feet as well) is common.

2. Tachycardia frequently is present, blood pressure is decreased.

3. Poor skin tugor and dry skin may be prominent.

4. Hypothermia (when the normal body temperature for body metabolism is dropped, usually to 35 degrees Celsius) is common in LA.

5. Hyperpnea (increased depth of breathing when required to meet demand, as during or following exercise or when the body lacks oxygen- hypoxia) or Kussmaul respiration is present and related to degree of acidosis.

4. Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.

Laboratory findings

1. Blood glucose level is not high

2. Glucosurea (Glucose in Urine) is absent.

3. Blood lactic acid is high.

Treatment

LA is treated by correcting the underlying cause.

In severe cases, bicarbonate therapy should be used (intravenously-infused 2,5 % sodium bicarbonates 1 to 2 l/day).

LA can be treated with low dose insulin regimens with 5 % glucose solution infusion.

Volume expanders and oxygen therapy are helpful treatment as well.



Comparison of DCA, HNC and LA.

DKA

1. Age: Below 40 years

2. Type of DM: Type I

3. Predisposing factor: Insulin Deficiency

4. prodromes: Several days duration or less than 1 day

5. Underlying renal, Cardiovascular or Pulmonary disease: About 15%

6. General: More acidic and less dehydrated, hyperventilation

7. Neurologic symptoms and signs: rare

8. Laboratory findings: blood glucose- High (about 20-30 mmol/l)

9. Plasma Ketones: +

10. Serum bicarbonate: Low

11. Blood pH: Less than 7.35

12. Serum Osmolality: less than 330 mOsm?l

13. free fatty acids: elevated

14. serum sodium: Normal, elevated or low

15. Serum Potassium: Noraml, elevated or low

16. Complications-thrombosis: rare

17. Mortality rate: 1-10%

18. Diabetes treatment after recovery: Always Insulin


HNC

1. Age: Above 40

2. Type of DM: Type II

3. Predisposing factor: Dehydration

4. Prodromes: several days duration

5. Underlying renal, Cardiovascular or pulmonary diseases: 85%

6. General: More hydrated and less acidic, no hyperventilation

7. Neurologic symptoms: very common

8. Laboratory findings- blood glucose: very high (about 40-50 mmol/l)

9. Plasma Ketones: -

10. Serum sodium: Normal, elevated or low

11. Serum Potassium: Normal, elevated or low

12. Serum bicarbonate: Normal

13. Blood pH: Normal

14. Serum Osmolality: over 350 mOsm/l

15. free fatty acids: decreased or normal

16. complications (thrombosis): frequent

17. Mortality rate: 20-50%

18. Diabetes treatment after recovery: Diet alone or Oral agents and sometimes insulin.

LA

1. Age: Above 40

2. Type of DM: Type II

3. Predisposing factor: Hypoxia

4. Prodromes: Less than 1 day

5. Underlying renal, Cardiovascular or Pulmonary diseases: About 90%

6. General: More acidic and less dehydrated, hyperventilation

7. Neurologic symptoms and signs: Very common

8. Laboratory findings-blood glucose: Normal or about 10-11 mmol/l

9. Plasma ketones: -

10. Serum Sodium: Normal

11. Serum Potassium: Normal

12. Serum Bicarbonate: Low

13. Blood pH: Less than 7.35

14. Serum Osmolality: Normal

15. free fatty acids: Normal

16. Complications (thrombosis): very rare

17. Mortality rate: About 90%

18. Diabetes treatment: Diet alone or oral agents, sometimes insulin.

HYPOGLYCEMIA

It is a syndrome characterized by symptoms of sympathetic nervous system stimulation or central nervous system dysfunction that are provoked by an abnormally low plasma glucose level.

Hypoglycemia represents insulin excess and it can occur at any time.

Precipitating factors

- irregular ingestion of food;

- extreme activity;

- alcohol ingestion;

- drug interaction;

- liver or renal disease;

- hypopituitarism and adrenal insufficiency.

Clinical presentation

Signs and symptoms.

Two distinct patterns are distinguished:

1) adrenergic symptoms (they are attributed to increased sympathetic activity and epinephrine release): sweating, nervousness, tremulousness, faintness, palpitation, and sometimes hunger;

2) cerebral nervous system manifestations: confusion, inappropriate behavior (which can be mistaken for inebriation); visual disturbances, stupor, coma or seizures. (Improvement in the cerebral nervous system manifestations will be with a rise in blood glucose.)

A common symptom of hypoglycemia is the early morning headache, which is usually present when the patient awakes.

Patients should be familiar with the symptoms of the hypoglycemia but some of them are not heralded by symptoms.

Physical examination.

1. The skin is cold, moist.

2. Hyperreflexia can be elicited.

3. Hypoglycemic coma is commonly associated with abnormally low body temperature

4. Patient may be unconsciousness.

Laboratory findings

1. Low level of blood glucose

Treatment

Insulin–treated patients are advised to carry sugar lumps, candy, or glucose tablets at all time.

If the symptoms of hypoglycemia develop, the patients have to drink a glass of fruit juice or water with 3 tbsp. of table sugar added or to eat candy, and to teach their family members to give such treatment if they suddenly exhibit confusion or inappropriate behavior:

1) Glucagons 0,5 – 1 unit (0,5 – 1 ml) s/c, i/m or i/v. If the patient does not respond to 1 unit of glucagon within 25 minutes, further injections are unlikely to be effective, and are not recommended;

2) an i/v injection of 20 or 100 ml of 40 % glucose, followed by a continuous infusion of 5 % glucose (10 % glucose may be needed) until it clearly can be stopped safely;

3) glucocorticoids and adrenaline are helpful as well.


You can check out my previous hub on Diabetes mellitus here

More by this Author


Comments 36 comments

Dr. Felix Boadi-Danquah 6 years ago

A very and truly great hub. Keep it up the Virtual Doctor, and very soon I will be here to ask some questions. What is with the serious urinating (ha ha ha ha ha ha ha ha ha ha)? Its really hilarious.


The American Heart 6 years ago

How is diabetes treated?

When diabetes is detected, a doctor may prescribe changes in eating habits, weight control and exercise programs, and even drugs to keep it in check. It's critical for people with diabetes to have regular checkups. Work closely with your healthcare provider to manage diabetes and control any other risk factors. For example, blood pressure for people with diabetes and high blood pressure should be lower than 130/80 mm Hg.

AHA Recommendation

Diabetes is a major risk factor for stroke and coronary heart disease, which includes heart attack. People with diabetes may avoid or delay heart and blood vessel disease by controlling the other risk factors. It's especially important to control weight and blood cholesterol with a low-saturated-fat, low-cholesterol diet and regular aerobic physical activity. It's also important to lower high blood pressure and not to smoke.


e-medicine 6 years ago

Symptoms of ketoacidosis

These symptoms include the following:

Severe dehydration

Smell of ketones

Acidotic breathing (ie, Kussmaul respiration), masquerading as respiratory distress

Abdominal pain

Vomiting

Drowsiness and coma

Other nonspecific findings include the following:

Hyperglycemia impairs immunity and renders a child more susceptible to recurrent infection, particularly of the urinary tract, skin, and respiratory tract.

Candidiasis may develop, especially in groin and flexural areas.

Physical

Apart from wasting and mild dehydration, children with early diabetes have no specific clinical findings.

A physical examination may reveal findings associated with other autoimmune endocrinopathies, which have a higher incidence in children with type 1 diabetes mellitus (eg, thyroid disease with symptoms of overactivity or underactivity and possibly a palpable goiter).

Cataracts are rarely presenting problems and typically occur in girls with a long prodrome of mild hyperglycemia.

Necrobiosis lipoidica usually, but not exclusively, occurs in people with diabetes. Necrobiosis most often develops on the front of the lower leg as a well-demarcated, red, atrophic area. The condition is associated with injury to dermal collagen, granulomatous inflammation, and ulceration. The cause of necrobiosis is unknown, and the condition is difficult to manage. It is also associated with poor metabolic control and a greater risk of developing other diabetes-related complications.

Keep it up D.Virtual.Doctor! Its rated high


Why didn't you talk about Gestational Diabetes? 6 years ago

Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life.

Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.

A 2008 study completed in the U.S. found that the number of American women entering pregnancy with preexisting diabetes is increasing. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years.[7] This is particularly problematic as diabetes raises the risk of complications during pregnancy, as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future.


Tutorials on Diabetes 6 years ago

Wow! So many clinical comments here. The last time I checked, you published this article just today! This is nice, I think such an information is very rare to find. People just talk about Diabetes, its complications and that's it! In your previous hub, I had to learn about DM complications on the male and female sexuality, here are some tips from us about Diabetes

Pancreas

The islets of Langerhans are destroyed in type I diabetes mellitus. This occurs probably as a consequence of a genetic susceptibility, followed by the onset of autoimmune destruction triggered by some environmental factor such as a viral infection. Heavy lymphocytic infiltrates appear in and around islets. The number and size of islets are eventually reduced, leading to decreased insulin production and glucose intolerance.

The islets of Langerhans are normal in number or somewhat reduced with type II diabetes mellitus. Fibrosis and deposition of amylin polypeptide within islets are most characteristic of the chronic states of type II diabetes.

Normal islets of Langerhans, with immunoperoxidase stains (right, insulin and left, glucagon), microscopic.

Islet of Langerhans, insulitis, microscopic.

Islet of Langerhans, deposition of amyloid, microscopic.

Renal Complications

There are a variety of complications involving the kidney. Both nodular and diffuse glomerulosclerosis can lead to chronic renal failure. Diabetics are prone to infections, particularly pyelonephritis. Both bacterial and fungal infections can occur.

Renal glomerulus, nodular glomerulosclerosis, microscopic.

Renal glomerulus, nodular glomerulosclerosis, hyaline arteriolosclerosis, PAS stain, microscopic.

Kidney, acute pyelonephritis, microscopic.

Renal pelvis, infection with Candida albicans, PAS stain, microscopic.

Ocular Complications

The eyes can be affected in several ways by diabetes mellitus. Diabetic retinopathy is one of the leading causes for irreversible blindness in the United States. This retinopathy can occur with either type I or type II diabetes mellitus, usually a decade or so after the onset of diabetes. Most persons with type I diabetes and many of those with type II diabetes develop some background (non-proliferative ) retinopathy. Proliferative retinopathy is more ominous and is more likely to occur when diabetes mellitus is poorly controlled.

In severe retinopathy, neovascularization may lead to adhesions (synechiae) between iris and cornea or iris and lens. Neovascularization of the iris leads to secondary glaucoma with blindness.

Cataracts are more common in diabetics. This predilection for development of cataracts is felt to result from hyperglycemia leading to accumulation of sorbitol that results in osmotic damage to the crystalline lens.

Normal appearance, retina on funduscopic examination.

Diabetic retinopathy on funduscopic examination.

Proliferative diabetic retinopathy on funduscopic examination.

Glaucoma, cupping of the optic disk on funduscopic examination.

Glaucoma with excavation of the optic cup, microscopic.

Cataract of the crystalline lens, gross.

Atherosclerosis

Persons with diabetes mellitus, either type I or type II, have early and accelerated atherosclerosis. The most serious complications of this are atherosclerotic heart disease, cerebrovascular disease, and renal disease. The most common cause of death with diabetes mellitus is myocardial infarction.

Peripheral vascular disease is a particular problem with diabetes mellitus and is made worse through the development of diabetic neuropathy, leading to propensity for injury.

Left anterior descending coronary artery, advanced atherosclerosis, gross.

Left anterior descending coronary artery, recent thrombus, microscopic.

Interventricular septum, recent myocardial infarction, gross.

Aortic atherosclerosis demonstrated in three aortas, gross.

Foot with previous healed transmetatarsal amputation and recent ulcer, gross.

Gangrenous necrosis and ulceration, lower extremity, gross.

Mucormycosis

This is a feared complication of diabetes mellitus. Diabetic ketoacidosis helps to potentiate the growth of Mucor. The site of involvement is typically the nasopharyngeal region, but the infection can spread to involve soft tissues and bone of the face, orbit, skull, and brain.

Keep the good work and try to visit our site, okay!


Come and get some treatments to Diabetes Mellitus 6 years ago

Insulin injections are not as perfect as the insulin produced by the pancreas. Blood sugar levels will not always be normal in diabetic pets. The goal of treatment is to reduce the signs of diabetes. When diabetes is well controlled with insulin, the pet should drink, eat and urinate normal amounts. They should have a good appetite, without becoming fat and should have normal activity.

Insulin needs are closely related to the type of food eaten by the pet. Your veterinarian will recommend a specific diet and feeding regimen that will enhance the effectiveness of insulin. If your pet is overweight, s(he) will be placed on a weight-reducing diet. As the pet loses weight, less insulin will be needed. Only feed the recommended diet..NO table scraps or treats that are not part of the recommended diet.

Heavy exercise will reduce the amount of insulin needed. It is important to talk to your veterinarian before making changes in diet or exercise.

There is always some risk that a diabetic patient will develop low blood sugar. Signs of low blood sugar include weakness, staggering, seizures, or just being more quiet than usual. You should keep corn syrup on hand to rub on the animals gums if they have signs suggestive of low blood sugar. Don't pour large amounts of corn syrup in the mouth of an animal that is not fully conscious as the syrup may be inhaled into the lungs.

Because insulin needs vary with the activity and lifestyle of your pet, you may want to keep a written daily log of:

the dose of insulin

location in which the insulin is injected

any changes in the pet’s activity or appetite

Your veterinarian may ask you to check your pet's urine for sugar using a test strip. If your pet is well regulated on insulin, the sugar readings in most urine samples will be negative or trace. The strips may have color pads only for glucose or for glucose and ketones.


Mayo Clinic 6 years ago

Type 1 diabetes signs and symptoms can come on quickly and may include:

Increased thirst and frequent urination. As excess sugar builds up in your bloodstream, fluid is pulled from your tissues. This may leave you thirsty. As a result, you may drink — and urinate — more than usual.

Extreme hunger. Without enough insulin to move sugar into your cells, your muscles and organs become depleted of energy. This triggers intense hunger that may persist even after you eat. Without insulin, the sugar in your food never reaches your energy-starved tissues.

Weight loss. Despite eating more than usual to relieve hunger, you may lose weight — sometimes rapidly. Without the energy sugar supplies, your muscle tissues and fat stores may simply shrink.

Fatigue. If your cells are deprived of sugar, you may become tired and irritable.

Blurred vision. If your blood sugar level is too high, fluid may be pulled from your tissues — including the lenses of your eyes. This may affect your ability to focus clearly.

When to see a doctor

Consult your doctor if you're concerned about diabetes or if you notice any type 1 diabetes signs and symptoms.

You are indeed outstanding...


Dchosen_01 6 years ago

Wow! This is unbelievable! Is this hub going viral already? Are you into SEO? Its really great to realize such a hub in a short time with great achievement already. Yeah! I think I agree with one of the comments here, it is very rare to find such a topic about diabetes. In fact, I never knew of such until I read your hub and It is a privilege for me to do more search on Ketoacidosis, Lactic acidosis and Hypoglycemic Coma. Great work I must say and now I see why you take time to publish one hub. I can only imagine 100 of such hubs in some month's time. It will be a blessing to this community and the hubpages administration as well.

Keep up the good work...


D.Virtual.Doctor profile image

D.Virtual.Doctor 6 years ago from Europe Author

wow! Guys! I can't really believe this. Well, that's why I am your virtual doctor. Thanks a lot Dchosen_01 (lol!) and also special thanks to all the Diabetics groups here. We are all in the same course creating awareness and helping the community be better equipped in terms of health. I am so happy to see the emmence cooperation between all stake holders involved. You guys have spur me to do more and do better. Really, this is an encouragement. I never would have thought I will get a response from Mayo Clinic! I never thought of this. But this is a sign of a great work and togetherness. As for you Dr. Felix, yeah, I kinda think its funny too. Really, I did not see it that way until you commented on it. Thanks and I hope the other Doctors will write their own comments too!


W.H.O 6 years ago

Diabetes mellitus is a chronic disease which is difficult to cure. Management concentrates on keeping blood sugar levels as close to normal ("euglycemia") as possible without presenting undue patient danger. This can usually be with close dietary management, exercise, and use of appropriate medications (insulin only in the case of type 1 diabetes mellitus. Oral medications may be used in the case of type 2 diabetes, as well as insulin).

Patient education, understanding, and participation is vital since the complications of diabetes are far less common and less severe in people who have well-managed blood sugar levels.[17][18] Wider health problems may accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise.

Lifestyle modifications

Main article: Diabetic diet

There are roles for patient education, dietetic support, sensible exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.

I can see that this article is a dwelling place for all interested parties involved in fighting this ailment. We register our comments here as well.

Good work D.Virtual.Doctor


American Diabetes Association 6 years ago

Your Weight and Your Risk

Being overweight raises your risk for type 2 diabetes, heart disease, and stroke. It can cause other problems, too, like high blood pressure, unhealthy cholesterol, and high blood glucose (sugar). Losing weight can help you prevent and manage these problems. And you don't have to lose a lot of weight. Even a loss of 10–15 pounds can make a big difference.

Getting Started

Weight loss can be hard because it means making changes in the way you eat and in your physical activity. Losing weight also takes time—and that can be frustrating. The good news is that you can lose weight and keep it off, even if you've never done it before.

Here's what works for people who have lost weight and kept it off:

They cut back on calories and fat.

They're physically active most days of the week.

They eat breakfast every day.

They keep a record of their weight, what they eat and drink, and what they do for physical activity.

It's much easier to lose weight when you change the way you eat and also increase your activity.

Learn more about changing habits, making healthier food choices, and getting started with physical activity.

Small Steps

Most people find it's easier to tackle changes in a few small steps instead of all at once. Set realistic goals within a timeframe that works for you. Learn more about making realistic, achievable goals.

Keep a Record

Many people find that writing everything down helps keep them on target. Try it even just for a week or two, to get an idea of where you stand.

Keep a small notebook with you all day. Write down everything you eat and drink, including the serving size. Some people set target levels for calories or grams of fat and keep track of their daily totals.

Make a note of what kind of physical activity you do and for how long. It may also help to write down other information, like when or where you exercised, who you exercised with, or how you felt before, during, or after exercise.

You may want to check your weight once a week and write it down, or use your clothes as a measure of weight loss.

Your Support System

Many people find it helpful to meet, online or in person, with people who are also trying to lose weight. Think about joining a group for weight loss, exercise, or general support. Or create your own support system by talking with friends and family about your successes and your struggles. You may be surprised at how supportive they will be.

Find a walking buddy or friends who also want to improve their health. Then work together to reach your goals.

Learn more about healthy weight loss.

Learn more about your risk for type 2 diabetes and heart disease.


Not, into Diabetes, just a passer-by 6 years ago

Diabetes mellitus: Better known just as "diabetes" -- a chronic disease associated with abnormally high levels of the sugar glucose in the blood. Diabetes is due to one of two mechanisms:

(1) Inadequate production of insulin (which is made by the pancreas and lowers blood glucose) or

(2) Inadequate sensitivity of cells to the action of insulin.

The two main types of diabetes correspond to these two mechanisms and are called insulin dependent (type 1) and non-insulin dependent (type 2) diabetes. In type 1 diabetes there is no insulin or not enough of it. In type 2 diabetes, there is generally enough insulin but the cells upon it should act are not normally sensitive to its action.

The signs and symptoms of both types of diabetes include increased urine output and decreased appetite as well as fatigue. Diabetes is diagnosed by blood glucose testing, the glucose tolerance test, and testing of the level of glycosylated hemoglobin (glycohemoglobin or hemoglobin A1C). The mode of treatment depends on the type of the diabetes.

The major complications of diabetes include dangerously elevated blood sugar, abnormally low blood sugar due to diabetes medications, and disease of the blood vessels which can damage the eye, kidneys, nerves, and heart.


Treatment of Diabetes Mellitus 6 years ago

The goal of diabetes management is to keep blood glucose levels as close to normal as safely possible. Since diabetes may greatly increase risk for heart disease and peripheral artery disease, measures to control blood pressure and cholesterol levels are an essential part of diabetes treatment as well.

People with diabetes must take responsibility for their day-to-day care. This includes monitoring blood glucose levels, dietary management, maintaining physical activity, keeping weight and stress under control, monitoring oral medications and, if required, insulin use via injections or pump. To help patients achieve this, UCSF's Diabetes Teaching Center offers self-management educational programs that emphasize individualized diabetes care. The program enables patients to make more consistent and appropriate adjustments in their therapy and lifestyle.

Dietary Management and Physical Activity

Modifying eating habits and increasing physical activity are typically the first steps toward reducing blood sugar levels. At UCSF Medical Center, all patients work with their doctor and certified dietician to develop a dietary plan. Our Teaching Center conducts workshops that provide patients with information on food nutrient content, healthy cooking and exercise.

Insulin Therapy

People with type 1 diabetes require multiple insulin injections each day to maintain safe insulin levels. Insulin is often required to treat type 2 diabetes too. Using an insulin pump is an alternative to injections. The pump is about the size of a pager and is usually worn on your belt. Insulin is delivered through a small tube (catheter) that is placed under the skin (usually in the abdomen).

There are four major types of insulin:

Rapid-acting

Short-acting

Intermediate-acting

Long-acting

Your doctor will determine your dose and how often you need to take insulin. There is no standard insulin dose as it depends on factors such as your body weight, when you eat, how often you exercise and how much insulin your body produces.

Oral Medications

Sometimes blood sugar levels remain high in people with type 2 diabetes even though they eat in a healthy manner and exercise. When this happens, medications taken in pill form may be prescribed. The medications work in several different ways. These include improve the effectiveness of the body's natural insulin, reduce blood sugar production, increase insulin production and inhibit blood sugar absorption. Oral diabetes medications are sometimes taken in combination with insulin.


Why is diabetes mellitus a National Health Priority Area? 6 years ago

Diabetes mellitus and its complications contribute significantly to ill health, disability, poor quality of life and premature death. Additionally, diabetes mellitus is a contributing factor to several other causes of morbidity and mortality. It also increases the risk of a variety of complications including end-stage kidney disease, coronary heart disease, stroke and other vascular diseases.

In 2003, diabetes was the eighth and tenth leading underlying cause of death in Australia among males (1,807) and females (1,582) respectively. It was also the fifth most frequently managed problem by general practitioners in Australia in 2003-04.

Diabetes mellitus was responsible for just under 5% of the burden of disease in disability-adjusted life years in Australia in 1996. In monetary terms, the direct costs of diabetes mellitus and its complications were estimated at $836 million in 2000-01 and this is expected to increase as the population ages.


al_masculine 6 years ago

wow!! You can publish another hub on Diabetes from all these professional comments. D.Virtual.Doctor, I do not understand! Are you in any diabetic group, or organization or association? There is no doubt you did very great in your hub. That's good. Keep it up...


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D.Virtual.Doctor 6 years ago from Europe Author

Thanks guys! Just 1 hour after publishing and this is what it has resulted to. This indicates the need to be aware of this ailment. It is a serious problem to man-kind and a real threat to heath. Seriously, I am not in any diabetes group, I am just doing my thing out of my own idea and I think God is really helping me with success. Thanks every one and for those of you who want me to visit their websites, I will definitely do so.


Nell Rose profile image

Nell Rose 6 years ago from England

hi, Wow, you have certainly got of to a great start here! very good information and welcome to hubpages! thanks nell


boadinho profile image

boadinho 6 years ago

Hi, I take insulin jabs before b’fast ( 14 units ) and before dinner (6-8 units)

I take walks in the evening during sunset for about 30-40 mins 3 times a week.

Doc said my pancreas cant produce enough.

Am i a type 1 or type 2 diabetes???


D.Virtual.Doctor profile image

D.Virtual.Doctor 6 years ago from Europe Author

boadinho! You should have told me earlier on that you have a profile here. Seriously its great and nice to know you are connected here and I am waiting to read your publications. Inability of the pancreas to produce Insulin Indicates Diabetes Type I. SO, I think this is Diabetes Mellitus Type I. Can I also know your age?


al_masculine 6 years ago

hmmm! What a doctor!


al_masculine 6 years ago

hmmm! What a doctor!


Dr. Elenga Gift 6 years ago

Yeah, its Diabetes Type I


Dchosen_01 6 years ago

This is like a trophy, achieving such in just some few hours? Indeed very great...


stanford university medical center 6 years ago

Evaluating the results of the oral glucose tolerance test

Glucose tolerance tests may lead to one of the following diagnoses:

Normal response: A person is said to have a normal response when the 2-hour glucose level is less than 140 mg/dl, and all values between 0 and 2 hours are less than 200 mg/dl.

Impaired glucose tolerance: A person is said to have impaired glucose tolerance when the fasting plasma glucose is less than 126 mg/dl and the 2-hour glucose level is between 140 and 199 mg/dl.

Diabetes: A person has diabetes when two diagnostic tests done on different days show that the blood glucose level is high.

Gestational diabetes: A woman has gestational diabetes when she has any two of the following: a 100g OGTT, a fasting plasma glucose of more than 95 mg/dl, a 1-hour glucose level of more than 180 mg/dl, a 2-hour glucose level of more than 155 mg/dl, or a 3-hour glucose level of more than 140 mg/dl.


university of california--los angeles geffen david geffen school of medicine 6 years ago

Why is blood sugar checked at home?

Home blood sugar (glucose) testing is an important part of controlling blood sugar. One important goal of diabetes treatment is to keep the blood glucose levels near the normal range of 70 to 120 mg/dl before meals and under 140 mg/dl at two hours after eating. Blood glucose levels are usually tested before and after meals, and at bedtime. The blood sugar level is typically determined by pricking a fingertip with a lancing device and applying the blood to a glucose meter, which reads the value. There are many meters on the market, for example, Accu-Check Advantage, One Touch Ultra, Sure Step and Freestyle. Each meter has its own advantages and disadvantages (some use less blood, some have a larger digital readout, some take a shorter time to give you results, etc). The test results are then used to help patients make adjustments in medications, diets, and physical activities.

There are some interesting developments in blood glucose monitoring. Currently, at least three continuous glucose sensors are approved in the United States (Dexcom, Medtronic and Navigator). The new continuous glucose sensor systems involve an implantable cannula placed just under the skin in the abdomen or in the arm. This cannula allows for frequent sampling of blood glucose levels. Attached to this is a transmitter that sends the data to a pager-like device. This device has a visual screen that allows the wearer to see, not only the current glucose reading, but also the graphic trends. In some devices, the rate of change of blood sugar is also shown. There are alarms for low and high sugar levels. Certain models will alarm if the rate of change indicates the wearer is at risk for dropping or rising blood glucose too rapidly. The Medtronic version is specifically designed to interface with their insulin pumps. However, at this time the patient still must manually approve any insulin dose (the pump cannot blindly respond to the glucose information it receives, it can only give a calculated suggestion as to whether the wearer should give insulin, and if so, how much). All of these devices need to be correlated to fingersticks for a few hours before they can function independently. The devices can then provide readings for 3-5 days.

Diabetes experts feel that these blood glucose monitoring devices give patients a significant amount of independence to manage their disease process; and they are a great tool for education as well. It is also important to remember that these devices can be used intermittently with fingersticks. For example, a well-controlled patient with diabetes can rely on fingerstick glucose checks a few times a day and do well. If they become ill, if they decide to embark on a new exercise regimen, if they change their diet and so on, they can use the sensor to supplement their fingerstick regimen, providing more information on how they are responding to new lifestyle changes or stressors. This kind of system takes us one step closer to closing the loop, and to the development of an artifical pancreas that senses insulin requirements based on glucose levels and the body's needs and releases insulin accordingly - the ultimate goal.


university of chicago pritzker school of medicine 6 years ago

Hemoglobin A1c (A1c)

To explain what a hemoglobin A1c is, think in simple terms. Sugar sticks, and when it's around for a long time, it's harder to get it off. In the body, sugar sticks too, particularly to proteins. The red blood cells that circulate in the body live for about three months before they die off. When sugar sticks to these cells, it gives us an idea of how much sugar is around for the preceding three months. In most labs, the normal range is 4%-5.9 %. In poorly controlled diabetes, its 8.0% or above, and in well controlled patients it's less than 7.0% (optimal is


university of pittsburgh school of medicine 6 years ago

What are the acute complications of diabetes?

Severely elevated blood sugar levels due to an actual lack of insulin or a relative deficiency of insulin.

Abnormally low blood sugar levels due to too much insulin or other glucose-lowering medications.

Insulin is vital to patients with type 1 diabetes - they cannot live with out a source of exogenous insulin. Without insulin, patients with type 1 diabetes develop severely elevated blood sugar levels. This leads to increased urine glucose, which in turn leads to excessive loss of fluid and electrolytes in the urine. Lack of insulin also causes the inability to store fat and protein along with breakdown of existing fat and protein stores. This dysregulation, results in the process of ketosis and the release of ketones into the blood. Ketones turn the blood acidic, a condition called diabetic ketoacidosis (DKA). Symptoms of diabetic ketoacidosis include nausea, vomiting, and abdominal pain. Without prompt medical treatment, patients with diabetic ketoacidosis can rapidly go into shock, coma, and even death.

Diabetic ketoacidosis can be caused by infections, stress, or trauma all which may increase insulin requirements. In addition, missing doses of insulin is also an obvious risk factor for developing diabetic ketoacidosis. Urgent treatment of diabetic ketoacidosis involves the intravenous administration of fluid, electrolytes, and insulin, usually in a hospital intensive care unit. Dehydration can be very severe, and it is not unusual to need to replace 6-7 liters of fluid when a person presents in diabetic ketoacidosis. Antibiotics are given for infections. With treatment, abnormal blood sugar levels, ketone production, acidosis, and dehydration can be reversed rapidly, and patients can recover remarkably well.

In patients with type 2 diabetes, stress, infection, and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Accompanied by dehydration, severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). This condition can lead to coma (hyperosmolar coma). A hyperosmolar coma usually occurs in elderly patients with type 2 diabetes. Like diabetic ketoacidosis, a hyperosmolar coma is a medical emergency. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. Unlike patients with type 1 diabetes, patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. Since in general, type 2 diabetes occurs in an older population, concomitant medical conditions are more likely to exist, and these patients may actually be sicker overall. The complication and death rates from hyperosmolar coma is thus higher than in DKA.

Hypoglycemia means abnormally low blood sugar (glucose). In patients with diabetes, the most common cause of low blood sugar is excessive use of insulin or other glucose-lowering medications, to lower the blood sugar level in diabetic patients in the presence of a delayed or absent meal. When low blood sugar levels occur because of too much insulin, it is called an insulin reaction. Sometimes, low blood sugar can be the result of an insufficient caloric intake or sudden excessive physical exertion.

Blood glucose is essential for the proper functioning of brain cells. Therefore, low blood sugar can lead to central nervous system symptoms such as:

dizziness,

confusion,

weakness, and

tremors.

The actual level of blood sugar at which these symptoms occur varies with each person, but usually it occurs when blood sugars are less than 65 mg/dl. Untreated, severely low blood sugar levels can lead to coma, seizures, and, in the worse case scenario, irreversible brain death. At this point, the brain is suffering from a lack of sugar, and this usually occurs somewhere around levels of


vanderbilt university school of medicine 6 years ago

What are the chronic complications of diabetes?

These diabetes complications are related to blood vessel diseases and are generally classified into small vessel disease, such as those involving the eyes, kidneys and nerves (microvascular disease), and large vessel disease involving the heart and blood vessels (macrovascular disease). Diabetes accelerates hardening of the arteries (atherosclerosis) of the larger blood vessels, leading to coronary heart disease (angina or heart attack), strokes, and pain in the lower extremities because of lack of blood supply (claudication).


cornell university weill medical college 6 years ago

Eye Complications

The major eye complication of diabetes is called diabetic retinopathy. Diabetic retinopathy occurs in patients who have had diabetes for at least five years. Diseased small blood vessels in the back of the eye cause the leakage of protein and blood in the retina. Disease in these blood vessels also causes the formation of small aneurysms (microaneurysms), and new but brittle blood vessels (neovascularization). Spontaneous bleeding from the new and brittle blood vessels can lead to retinal scarring and retinal detachment, thus impairing vision.

To treat diabetic retinopathy a laser is used to destroy and prevent the recurrence of the development of these small aneurysms and brittle blood vessels. Approximately 50% of patients with diabetes will develop some degree of diabetic retinopathy after 10 years of diabetes, and 80% of diabetics have retinopathy after 15 years of the disease. Poor control of blood sugar and blood pressure further aggravates eye disease in diabetes.

Cataracts and glaucoma are also more common among diabetics. It is also important to note that since the lens of the eye lets water through, if blood sugar concentrations vary a lot, the lens of the eye will shrink and swell with fluid accordingly. As a result, blurry vision is very common in poorly controlled diabetes. Patients are usually discouraged from getting a new eyeglass prescription until their blood sugar is controlled. This allows for a more accurate assessment of what kind of glasses prescription is required.


Mount Sinai School of Medicine 6 years ago

What can be done to slow diabetes complications?

Findings from the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS) have clearly shown that aggressive and intensive control of elevated levels of blood sugar in patients with type 1 and type 2 diabetes decreases the complications of nephropathy, neuropathy, retinopathy, and may reduce the occurrence and severity of large blood vessel diseases. Aggressive control with intensive therapy means achieving fasting glucose levels between 70-120 mg/dl; glucose levels of less than 160 mg/dl after meals; and a near normal hemoglobin A1C levels (see below).

Studies in type 1 patients have shown that in intensively treated patients, diabetic eye disease decreased by 76%, kidney disease decreased by 54%, and nerve disease decreased by 60%. More recently the EDIC trial has shown that type 1 diabetes is also associated with increased heart disease, similar to type 2 diabetes. However, the price for aggressive blood sugar control is a two to three fold increase in the incidence of abnormally low blood sugar levels (caused by the diabetes medications). For this reason, tight control of diabetes to achieve glucose levels between 70-120 mg/dl is not recommended for children under 13 years of age, patients with severe recurrent hypoglycemia, patients unaware of their hypoglycemia, and patients with far advanced diabetes complications. To achieve optimal glucose control without an undue risk of abnormally lowering blood sugar levels, patients with type 1 diabetes must monitor their blood glucose at least four times a day and administer insulin at least three times per day. In patients with type 2 diabetes, aggressive blood sugar control has similar beneficial effects on the eyes, kidneys, nerves and blood vessels.


northwestern university feinberg school of medicine 6 years ago

Diabetes At A Glance

Diabetes is a chronic condition associated with abnormally high levels of sugar (glucose) in the blood.

Insulin produced by the pancreas lowers blood glucose.

Absence or insufficient production of insulin causes diabetes.

The two types of diabetes are referred to as type 1 (insulin dependent) and type 2 (non-insulin dependent).

Symptoms of diabetes include increased urine output, thirst and hunger as well as fatigue.

Diabetes is diagnosed by blood sugar (glucose) testing.

The major complications of diabetes are both acute and chronic.

Acutely: dangerously elevated blood sugar, abnormally low blood sugar due to diabetes medications may occur.

Chronically: disease of the blood vessels (both small and large) which can damage the eye, kidneys, nerves, and heart may occur

Diabetes treatment depends on the type and severity of the diabetes. Type 1 diabetes is treated with insulin, exercise, and a diabetic diet. Type 2 diabetes is first treated with weight reduction, a diabetic diet, and exercise. When these measures fail to control the elevated blood sugars, oral medications are used. If oral medications are still insufficient, insulin medications are considered.


case western reserve university (some patients remarks)school of medicine 6 years ago

My blood glucose lab readings for 49 years were always between 99 and 104. I had the last test done 5 days before entering the hospital for a "spider bite" which turned out to be MRSA. My glucose levels were 500-600. I had no symptoms and since I'd never been hospitalized, it actually felt like a "spa" to me - no cooking, no phones, etc. I was loving this. Well, I wound up having severe surgery removing a rather large mass from my upper thigh. I was put on Glucophage the minute the sugar levels were notices elevated. My docs (from one of the world's most famous hospital) actually believe that the MRSA brought on the diabetes and in 3-4 months it will slowly dissipate. I've always eaten a very healthy, balanced diet. But the numbers jump from 103 to 500 every single day - no matter what I eat, when I take the meds, when I exercise, etc. BUT IT STILL HAVE NO SYMPTOMS! However, just because I can't "feel" it, I take this very seriously. Good luck to all.

Published: October 13 ::

Comment from: SSpumpkin, 65-74 Female (Patient)

After reviewing a letter written by my doctor, where I read he had prescribed Celebrex for me due to pain of Arthritis which had really messed up my neck, back and knees, I found that one of the side effects of Celebrex is Diabetes. I have Type 2, now, and have been being treated for it for over three years. I am keeping it under control, but it's not easy and I have a tendency to mess up when I cannot afford my medications. I am retired, living on a fixed income and money is hard to come by. As noted in the Celebrex info, this can also work into hypoglycemia. Just loads of fun here, huh?

Published: September 25 ::


emory university school of medicine (some patients remarks) 6 years ago

I was 8 yrs old. Had typical symptoms of thirst, lethargy, urinary frequency, weighed just 40 lb for 18 months, growing but getting thinner? TV hurt my eyes, no saliva and horrible taste in mouth, would sleep 24/7 if allowed to. The doctor kept insisting I was fine and did not examine me. A friend suggested it might be diabetes, but the doctor didn't want to test urine. He finally agreed to give me the test, but still insisting it would be negative. Wrong! I was referred to hospital for routine appointment in 2 weeks. Fortunately the school nurse said don't wait, go there now. Hospital doctors said I was 2 days from a coma.

Published: August 04 ::

Hearing loss , ringing in the ears and dehydration were my diabetic symptoms. Also sometimes my blood sugar would drop too low (40-) and I would have hypoglycemia. Also I had bladder infections that my doctor put down to menopause symptoms at first. I also have connective tissue disease which muddied the waters a bit until random blood work with my rheumatologist and my gynecologist showed elevated glucose levels. I have nine siblings and six out of 10 have diabetes. The first diagnosed was my youngest brother who died of diabetes complications age 35. I have told my four siblings who are not diagnosed yet to watch for symptoms of diabetes. They are not the youngest, my oldest sibling is free of symptoms. It might also be noted there are four different kinds of auto-immune disease with myself and my siblings.

Published: May 27 ::

Comment from: gibsongothchick, 25-34 Female (Patient)

My first diabetes symptom was diabetic neuropathy. I didn't know I was diabetic until I went to my doctor complaining about constant foot pain. After a multitude of tests for everything from rheumatoid arthritis to muscular dystrophy, an emergency room physician checked my blood sugar.

Published: November 24 ::

Comment from: Joanie, 45-54 Female (Patient)

The only symptom that I had was tingling in my legs especially at night after I retired to bed. The tingling became more severe where I could not get them to stop. I thought I had restless leg syndrome. My doctor tested me for diabetes and found that I had type II diabetes and the sugar was attacking my legs because it had no place to go. He put me on a sugar free diet and Actos and within one to two days my symptom were gone.

Published: October 24 ::

Comment from: rocky57, 45-54 Female (Patient)

My father's entire family has diabetes, so I knew to watch for symptoms as I aged. I did not, however, know the extent that diabetes can effect your dental health. I have had perfect teeth my entire life. At age 51, I went for a routine bi-annual cleaning, and was told I had beginning periodontal disease. The next week I was diagnosed with type2 diabetes.

Published: October 24 ::

Comment from: carr97, 25-34 Female (Patient)

I didn't have diabetes symptoms per se, but my mother was diagnosed with diabetes two months before I was. I went to see the doctor with a fractured wrist and when he took my history, I told him about my mother, and me being overweight, he tested me that same week. I had it too. Now both my mother and I are always looking, reading and studying up on as much information as we can on "our" disease. She helps me, and I help her.

Published: September 17 ::


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D.Virtual.Doctor 6 years ago from Europe Author

My lord and my God! What else can I say? Is there anything short or lacking about this Internet Hospital? There is immense growth and I am really proud of it. I just cannot imagine how this place would be in the next 3, 4, 5 and even 20 years. Thanks so much to all the US Med schools and Hospitals who contributed here.


Peter Leeper profile image

Peter Leeper 4 years ago from Londonderry, New Hampshire

Amazing Hub Doc! I noticed you read my hub about Signs of Diabetes and just added a link to this article for people who want to see a great write up on the complications for diabetics of all sorts! Thanks for putting it together!


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D.Virtual.Doctor 4 years ago from Europe Author

Thanks Peter, I appreciate it!

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