Symptoms of high blood sugar including increased thirst (polydipsia), increased volume of urination (polyurea), and increase hunger (polyphagia).

Symptoms of HHS include:

- Altered level of consciousness

- Neurologic signs including: blurred vision, headaches, focal seizures, myoclonic jerking, reversible paralysis

- Motor abnormalities including flaccidity, depressed reflexes, tremors or fasiciculations

- Hyperviscosity and increased risk of blood clot formation

- Dehydration

- Weight loss

- Nausea, vomiting, and abdominal pain

- Weakness

- Low blood pressure with standing

Hyperosmolar syndrome may take a long duration - days and weeks - to develop. However, certain signs and symptoms may indicate that such a condition is developing. Some of the signs include the following:

1. Excessive thirst despite frequently taking water / other liquids

2. Continued high level of blood sugar

3. Dry and/ or parched mouth

4. Frequency of urination increases

5. Pulse rate becomes rapid

6. Shortness of breath with exertion

7. Skin becomes dry and warm and there is no sweating

8. Sleepiness and/ or a condition of confusion

The major differential diagnosis is diabetic ketoacidosis (DKA). In contrast to DKA, serum glucose levels in HHS are extremely high, usually greater than 40-50 mmol/L (600 mg/dL). Metabolic acidosis is absent or mild. A temporary state of confusion (delirium) is also more common in HHS than DKA. HHS also tends to affect older people more. DKA may have fruity breath, and rapid and deep breathing.

DKA often has serum glucose level greater than 300 mg/dL (HHS is >600 mg/dL). DKA usually occurs in type 1 diabetics whereas HHS is more common in type 2 diabetics. DKA is characterized by a rapid onset, and HHS occurs gradually over a few days. DKA also is characterized by ketosis due to the breakdown of fat for energy.

Both DKA and HHS may show symptoms of dehydration, increased thirst, increased urination, increased hunger, weight loss, nausea, vomiting, abdominal pain, blurred vision, headaches, weakness, and low blood pressure with standing.

The degree of hyperglycemia can change over time depending on the metabolic cause, for example, impaired glucose tolerance or fasting glucose, and it can depend on treatment. Temporary hyperglycemia is often benign and asymptomatic. Blood glucose levels can rise well above normal and cause pathological and functional changes for significant periods without producing any permanent effects or symptoms. During this asymptomatic period, an abnormality in carbohydrate metabolism can occur which can be tested by measuring plasma glucose. However, chronic hyperglycemia at above normal levels can produce a very wide variety of serious complications over a period of years, including kidney damage, neurological damage, cardiovascular damage, damage to the retina or damage to feet and legs. Diabetic neuropathy may be a result of long-term hyperglycemia. Impairment of growth and susceptibility to certain infection can occur as a result of chronic hyperglycemia.

Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). It is most often seen in persons who have uncontrolled insulin-dependent diabetes.

The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad:

- Polyphagia – frequent hunger, especially pronounced hunger

- Polydipsia – frequent thirst, especially excessive thirst

- Polyuria – increased volume of urination (not an increased frequency for urination)

- Blurred vision

- Fatigue

- Restlessness

- Weight loss

- Poor wound healing (cuts, scrapes, etc.)

- Dry mouth

- Dry or itchy skin

- Tingling in feet or heels

- Erectile dysfunction

- Recurrent infections, external ear infections (swimmer's ear)

- Cardiac arrhythmia

- Stupor

- Coma

- Seizures

Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response. This hunger is not usually as pronounced as in Type I diabetes, especially the juvenile onset form, but it makes the prescription of oral hypoglycemic medication difficult to manage.

Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys, which leads to the presence of glucose in the urine. This produces an osmotic diuresis.

Signs and symptoms of diabetic ketoacidosis may include:

- Ketoacidosis

- Kussmaul hyperventilation: deep, rapid breathing

- Confusion or a decreased level of consciousness

- Dehydration due to glycosuria and osmotic diuresis

- Acute hunger and/or thirst

- 'Fruity' smelling breath odor

- Impairment of cognitive function, along with increased sadness and anxiety

Hyperglycemia caused a decrease in cognitive performance, specifically in processing speed, and executive function and performance. Decreased cognitive performance may cause forgetfulness and concentration loss

The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels). In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as "Kussmaul respiration"). The abdomen may be tender to the point that an acute abdomen may be suspected, such as acute pancreatitis, appendicitis or gastrointestinal perforation. Coffee ground vomiting (vomiting of altered blood) occurs in a minority of people; this tends to originate from erosion of the esophagus. In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness).

On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, tachycardia (a fast heart rate) and low blood pressure may be observed. Often, a "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. If Kussmaul respiration is present, this is reflected in an increased respiratory rate.

Small children with DKA are relatively prone to cerebral edema (swelling of the brain tissue), which may cause headache, coma, loss of the pupillary light reflex, and progress to death. It occurs in 0.3–1.0% of children with DKA, and has been described in young adults, but is overall very rare in adults. It carries a 20–50% mortality.

In untreated hyperglycemia, a condition called ketoacidosis may develop because decreased insulin levels increase the activity of hormone sensitive lipase. The degradation of triacylglycerides by hormone-sensitive lipase produces free fatty acids that are eventually converted to acetyl-coA by beta-oxidation.

Ketoacidosis is a life-threatening condition which requires immediate treatment. Symptoms include: shortness of breath, breath that smells fruity (such as pear drops), nausea and vomiting, and very dry mouth.

Chronic hyperglycemia (high blood sugar) injures the heart in patients without a history of heart disease or diabetes and is strongly associated with heart attacks and death in subjects with no coronary heart disease or history of heart failure.

Also, life-threatening consequences of hyperglycemia is nonketotic hyperosmolar syndrome.

Diabetic ketoacidosis (DKA), if it progresses and worsens without treatment, can eventually cause unconsciousness, from a combination of a very high blood sugar level, dehydration and shock, and exhaustion. Coma only occurs at an advanced stage, usually after 36 hours or more of worsening vomiting and hyperventilation.

In the early to middle stages of ketoacidosis, patients are typically flushed and breathing rapidly and deeply, but visible dehydration, pale appearance from diminished perfusion, shallower breathing, and a fast heart rate are often present when coma is reached. However these features are variable and not always as described.

If the patient is known to have diabetes, the diagnosis of DKA is usually suspected from the appearance and a history of 1–2 days of vomiting. The diagnosis is confirmed when the usual blood chemistries in the emergency department reveal a high blood sugar level and severe metabolic acidosis.

Treatment of DKA consists of isotonic fluids to rapidly stabilize the circulation, continued intravenous saline with potassium and other electrolytes to replace deficits, insulin to reverse the ketoacidosis, and careful monitoring for complications.

People with type 1 diabetes mellitus who must take insulin in full replacement doses are most vulnerable to episodes of hypoglycemia. It is usually mild enough to reverse by eating or drinking carbohydrates, but blood glucose occasionally can fall fast enough and low enough to produce unconsciousness before hypoglycemia can be recognized and reversed. Hypoglycemia can be severe enough to cause unconsciousness during sleep. Predisposing factors can include eating less than usual or prolonged exercise earlier in the day. Some people with diabetes can lose their ability to recognize the symptoms of early hypoglycemia.

Unconsciousness due to hypoglycemia can occur within 20 minutes to an hour after early symptoms and is not usually preceded by other illness or symptoms. Twitching or convulsions may occur. A person unconscious from hypoglycemia is usually pale, has a rapid heart beat, and is soaked in sweat: all signs of the adrenaline response to hypoglycemia. The individual is not usually dehydrated and breathing is normal or shallow. Their blood sugar level, measured by a glucose meter or laboratory measurement at the time of discovery, is usually low but not always severely, and in some cases may have already risen from the nadir that triggered the unconsciousness.

Unconsciousness due to hypoglycemia is treated by raising the blood glucose with intravenous glucose or injected glucagon.

Hyperosmolar syndrome or diabetic hyperosmolar syndrome is a medical emergency caused by a very high blood glucose level.

The prefix "hyper" means high, and "osmolarity" is a measure of the concentration of active particles in a solution, so the name of the syndrome simply refers to the high concentration of glucose in the blood.

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes.

DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.

The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.

Rates of DKA vary around the world. 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. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost universally fatal. The risk of death with adequate and timely treatment is currently around 1–4%. Up to 1% of children with DKA develop a complication known as cerebral edema.

Diabetic coma is a medical emergency in which a person with diabetes mellitus is comatose (unconscious) because of one of the acute complications of diabetes:

1. Severe diabetic hypoglycemia

2. Diabetic ketoacidosis advanced enough to result in unconsciousness from a combination of severe hyperglycemia, dehydration and shock, and exhaustion

3. Hyperosmolar nonketotic coma in which extreme hyperglycemia and dehydration alone are sufficient to cause unconsciousness.

Diabetic ketoacidosis (DKA) is an acute and dangerous complication that is always a medical emergency and requires prompt medical attention. Low insulin levels cause the liver to turn fatty acid to ketone for fuel (i.e., ketosis); ketone bodies are intermediate substrates in that metabolic sequence. This is normal when periodic, but can become a serious problem if sustained. Elevated levels of ketone bodies in the blood decrease the blood's pH, leading to DKA. On presentation at hospital, the patient in DKA is typically dehydrated, and breathing rapidly and deeply. Abdominal pain is common and may be severe. The level of consciousness is typically normal until late in the process, when lethargy may progress to coma. Ketoacidosis can easily become severe enough to cause hypotension, shock, and death. Urine analysis will reveal significant levels of ketone bodies (which have exceeded their renal threshold blood levels to appear in the urine, often before other overt symptoms). Prompt, proper treatment usually results in full recovery, though death can result from inadequate or delayed treatment, or from complications (e.g., brain edema). Ketoacidosis is much more common in type 1 diabetes than type 2.

Some common symptoms are:

- depression or lethargy

- confusion or dizziness

- trembling

- weakness

- ataxia (loss of coordination or balance)

- loss of excretory or bladder control (sudden house accident)

- vomiting, and then loss of consciousness and possible seizures

Successful home treatment of a hypoglycemia event depends on being able to recognize the symptoms early and responding quickly with treatment. Trying to make a seizing or unconsicous animal swallow can cause choking on the food or liquid. There is also a chance that the materials could be aspirated (enter the lungs instead of being swallowed). Seizures or loss of consciousness because of low blood glucose levels are medical emergencies.

The main sign of metabolic syndrome is central obesity (also known as visceral, male-pattern or apple-shaped adiposity), overweight with adipose tissue accumulation particularly around the waist and trunk.

Other signs of metabolic syndrome include high blood pressure, decreased fasting serum HDL cholesterol, elevated fasting serum triglyceride level (VLDL triglyceride), impaired fasting glucose, insulin resistance, or prediabetes.

Associated conditions include hyperuricemia, fatty liver (especially in concurrent obesity) progressing to nonalcoholic fatty liver disease, polycystic ovarian syndrome (in women), erectile dysfunction (in men), and acanthosis nigricans.

Hypoglycemia, or low blood glucose, can happen even with care, since insulin requirements can change without warning. Some common reasons for hypoglycemia include increased or unplanned exercise, illness, or medication interactions, where another medication the effects of the insulin. Vomiting and diarrhea episodes can bring on a hypoglycemia reaction, due to dehydration or simply a case of too much insulin and not enough properly digested food. Symptoms of hypoglycemia need to be taken seriously and addressed promptly. Since serious hypoglycemia can be fatal, it is better to treat a suspected incident than to fail to respond quickly to the signs of actual hypoglycemia. Dr. Audrey Cook addressed the issue in her 2007 article on diabetes mellitus: "Hypoglycemia is deadly; hyperglycemia is not. Owners must clearly understand that too much insulin can kill, and that they should call a veterinarian or halve the dose if they have any concerns about a pet's well-being or appetite. Tell owners to offer food immediately if the pet is weak or is behaving strangely."

The diagnostic criteria for steroid diabetes are those of diabetes (fasting glucoses persistently above 125 mg/dl (7 mM) or random levels above 200 mg/dl (11 mM)) occurring in the context of high-dose glucocorticoid therapy. Insulin levels are usually detectable, and sometimes elevated, but inadequate to control the glucose. In extreme cases the hyperglycemia may be severe enough to cause nonketotic hyperosmolar coma.

The approximate prevalence of the metabolic syndrome in patients with coronary heart disease (CHD) is 50%, with a prevalence of 37% in patients with premature coronary artery disease (age 45), particularly in women. With appropriate cardiac rehabilitation and changes in lifestyle (e.g., nutrition, physical activity, weight reduction, and, in some cases, drugs), the prevalence of the syndrome can be reduced.

Steroid diabetes (also "steroid-induced diabetes") is a medical term referring to prolonged hyperglycemia due to glucocorticoid therapy for another medical condition. It is usually, but not always, a transient condition.

The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss. Other symptoms that are commonly present at diagnosis include a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, and fatigue. Many people, however, have no symptoms during the first few years and are diagnosed on routine testing. A small number of people with type 2 diabetes mellitus can develop a hyperosmolar hyperglycemic state (a condition of very high blood sugar associated with a decreased level of consciousness and low blood pressure).

Low blood sugar is common in persons with type 1 and type 2 DM. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious issues such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases. Moderate hypoglycemia may easily be mistaken for drunkenness; rapid breathing and sweating, cold, pale skin are characteristic of hypoglycemia but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.

People (usually with type 1 DM) may also experience episodes of diabetic ketoacidosis, a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness.

A rare but equally severe possibility is hyperosmolar hyperglycemic state, which is more common in type 2 DM and is mainly the result of dehydration.

The classical symptoms of type 1 diabetes include: polyuria (excessive urination), polydipsia (increased thirst), dry mouth, polyphagia (increased hunger), fatigue, and weight loss.

Many type 1 diabetics are diagnosed when they present with diabetic ketoacidosis. The signs and symptoms of diabetic ketoacidosis include dry skin, rapid deep breathing, drowsiness, increased thirst, frequent urination, abdominal pain, and vomiting.

About 12 percent of people with type 1 diabetes have clinical depression.

About 6 percent of people with type 1 diabetes have celiac disease, but in most cases there are no digestive symptoms or are mistakenly attributed to poor control of diabetes, gastroparesis or diabetic neuropathy. In most cases, celiac disease is diagnosed after onset of type 1 diabetes. The association of celiac disease with type 1 diabetes increases the risk of complications, such as retinopathy and mortality. This association can be explained by shared genetic factors, and inflammation or nutritional deficiencies caused by untreated celiac disease, even if type 1 diabetes is diagnosed first.

Some people with type 1 diabetes experience dramatic and recurrent swings in glucose levels, often occurring for no apparent reason; this is called "unstable diabetes" or "labile diabetes", and sometimes "brittle diabetes", although this term is no longer used. The results of such swings can be irregular and unpredictable hyperglycemias, sometimes involving ketoacidosis, and sometimes serious hypoglycemias. Brittle diabetes occurs no more frequently than in 1% to 2% of diabetics.

The classic symptoms of untreated diabetes are weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 DM, while they usually develop much more slowly and may be subtle or absent in type 2 DM.

Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known ones above, they include blurry vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.

Diabetes mellitus type 1 (also known as type 1 diabetes) is a form of diabetes mellitus in which not enough insulin is produced. This results in high blood sugar levels in the body. The classical symptoms are frequent urination, increased thirst, increased hunger, and weight loss. Additional symptoms may include blurry vision, feeling tired, and poor healing. Symptoms typically develop over a short period of time.

The cause of type 1 diabetes is unknown. However, it is believed to involve a combination of genetic and environmental factors. Risk factors include having a family member with the condition. The underlying mechanism involves an autoimmune destruction of the insulin-producing beta cells in the pancreas. Diabetes is diagnosed by testing the level of sugar or A1C in the blood. Type 1 diabetes can be distinguished from type 2 by testing for the presence of autoantibodies.

There is no known way to prevent type 1 diabetes. Treatment with insulin is required for survival. Insulin therapy is usually given by injection just under the skin but can also be delivered by an insulin pump. A diabetic diet and exercise are an important part of management. Untreated, diabetes can cause many complications. Complications of relatively rapid onset include diabetic ketoacidosis and nonketotic hyperosmolar coma. Long-term complications include heart disease, stroke, kidney failure, foot ulcers and damage to the eyes. Furthermore, complications may arise from low blood sugar caused by excessive dosing of insulin.

Type 1 diabetes makes up an estimated 5–10% of all diabetes cases. The number of people affected globally is unknown, although it is estimated that about 80,000 children develop the disease each year. Within the United States the number of people affected is estimated at one to three million. Rates of disease vary widely with approximately 1 new case per 100,000 per year in East Asia and Latin America and around 30 new cases per 100,000 per year in Scandinavia and Kuwait. It typically begins in children and young adults.

Type 2 diabetes is typically a chronic disease associated with a ten-year-shorter life expectancy. This is partly due to a number of complications with which it is associated, including: two to four times the risk of cardiovascular disease, including ischemic heart disease and stroke; a 20-fold increase in lower limb amputations, and increased rates of hospitalizations. In the developed world, and increasingly elsewhere, type 2 diabetes is the largest cause of nontraumatic blindness and kidney failure. It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia. Other complications include acanthosis nigricans, sexual dysfunction, and frequent infections.

The symptoms of early and late dumping syndrome are different and vary from person to person. Early dumping syndrome symptoms may include:

- nausea

- vomiting

- abdominal pain and cramping

- diarrhea

- feeling uncomfortably full or bloated after a meal

- sweating

- weakness

- dizziness

- flushing, or blushing of the face or skin

- rapid or irregular heartbeat

The symptoms of late dumping syndrome may include:

- hypoglycemia

- sweating

- weakness

- rapid or irregular heartbeat

- flushing

- dizziness

About 75 percent of people with dumping syndrome report symptoms of early dumping syndrome and about 25 percent report symptoms of late dumping syndrome. Some people have symptoms of both types of dumping syndrome.