Acute Complications of Diabetes:
Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute complications of diabetes. DKA was formerly considered a hallmark of type 1 DM, but it also occurs in individuals who lack immunologic features of type IA DM and who can subsequently be treated with oral glucose-lowering agents (these individuals with type 2 DM are often of Hispanic or African-American descent).
HHS is primarily seen in individuals with type 2 DM. Both disorders are associated with absolute or relative insulin deficiency, volume depletion, and acid-base abnormalities.
DKA and HHS exist along a continuum of hyperglycemia, with or without ketosis.
Both disorders are associated with potentially serious complications if not promptly diagnosed and treated. The symptoms and physical signs of DKA usually develop over 24 hours. DKA may be the initial symptom complex that leads to a diagnosis of type 1 DM, but more frequently it occurs in individuals with established diabetes. Nausea and vomiting are often prominent, and their presence in an individual with diabetes warrants laboratory evaluation for DKA.
Abdominal pain may be severe and can resemble acute pancreatitis or ruptured viscous. Hyperglycemia leads to glucosuria, volume depletion, and tachycardia.
Hypotension can occur because of volume depletion in combination with peripheral vasodilation.
Kussmaul respirations and a fruity odor on the patient’s breathe (secondary to metabolic acidosis and increased acetone) are classic signs of the disorder.
Lethargy and central nervous system depression may evolve into coma with severe DKA but should also prompt evaluation for other reasons for altered mental status (infection, hypoxia, etc). Cerebral edema, an extremely serious complication of DKA, is seen most frequently in children. Signs of infection, which may precipitate DKA, should be sought on physical examination, even in the absence of fever.
Tissue ischemia (heart, brain) can also be a precipitating factor. Pathophgsiology of DKA results from relative or absolute insulin deficiency combined with counterregulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone). Both insulin deficiency and glucagon excess, in particular, are necessary for DKA to develop.
The decreased ratio of insulin to glucagon promotes gluconeogenesis, glycogenolysis, and ketone body formation in the liver, as well as increases in substrate delivery from fat and muscle (free fatty acids, amino acids) to the liver.
The combination of insulin deficiency and hyperglycemia reduces the hepatic level of fructose-2,6-phosphate, which alters the activity of phosphofructokinase and fructose- l,6-bisphosphatase .
Glucagon excess decreases the activity of pyruvate kinase, whereas insulin deficiency increases the activity of phosphoenolpyruvate carboxykinase. These changes shift the handling of pyruvate toward glucose synthesis and away from glycolysis. The increased levels of glucagon and catecholamines in the face of low insulin levels promote glycogenolysis .
Insulin deficiency also reduces levels of the GLUT4 glucose transporter, which impairs glucose uptake into skeletal muscle and fat and reduces intracellular glucose metabolism. Ketosis results from a marked increase in free fatty acid release from adipocytes, with a resulting shift towards ketone body synthesis in the liver.
Reduced insulin levels, in combination with elevations in catecholamines and growth hormone, increase lipolysis and the release of free fatty acids . Normally, these free fatty acids are converted to triglycerides or very low density lipoproteins (VLDL) in the liver.
However, in DKA, hyperglucagonemia alters hepatic metabolism to favor ketone body formation, through activation of the enzyme carnitine palmitoyltransferase I. This enzyme is crucial for regulating fatty acid transport into the mitochondria, where beta oxidation and conversion to ketone bodies occur. At physiologic pH, ketone bodies exist as ketoacids, which are neutralized by bicarbonate . As bicarbonate stores are depleted, metabolic acidosis ensues.
Increased lactic acid production also contributes to the acidosis. The increased free fatty acids increase triglyceride and VLDL production. VLDL clearance is also reduced because the activity of insulin-sensitive lipoprotein lipase in muscle and fat is decreased. Hypertriglyceridemia may be severe enough to cause pancreatitis.
DKA is initiated by inadequate levels of plasma insulin. Most commonly, DKA is precipitated by increased insulin requirements, as might occur during a concurrent illness. Failure to augment insulin therapy often compounds the problem.
Occasionally, complete omission of insulin by the patient or health care team (in a hospitalized patient with type 1 DM) precipitates DKA. Patients using insulin infusion devices with short-acting insulin are at increased risk of DKA, since even a brief interruption in insulin delivery (e.g., mechanical malfunction) quickly leads to insulin deficiency.
The timely diagnosis of DKA is crucial and allows for prompt initiation of therapy . DKA is characterized by hyperglycemia, ketosis, and metabolic acidosis(increased anion gap) along with a number of secondary metabolic derangements Occasionally, the serum glucose is only minimally elevated. Serum bicarbonate is frequently <I 0 mmol/L, and arterial pH ranges between 6 .8 and 7 .3, depending on the severity of the acidosis.
Despite a total-body potassium deficit, the serum potassium at presentation may be mildly elevated, secondary to the acidosis. Large changes occur during treatment of DKA.
Although plasma levels may be normal or high at presentation, total-body stores are usually depleted. Total-body stores of sodium, chloride, phosphorous, and magnesium are also reduced in DKA but are not accurately reflected by their levels in the serum because of dehydration and hyperglycemia. Elevated blood urea nitrogen (BUN) and serum creatinine levels reflect intravascular volume depletion.
Interference from acetoacetate may falsely elevate the serum creatinine measurement. Leukocytosis, hypertriglyceridemia, and hyperlipoproteinemia are commonly found as well. Hyperamylasemia may suggest a diagnosis of pancreatitis, especially when accompanied by abdominal pain. However, in DKA the amylase is usually of salivary origin and thus is not diagnostic of pancreatitis.
Serum lipase should be obtained if pancreatitis is suspected. The measured serum sodium is reduced as a consequence of the hyperglycemia [1 .6 mmol/L (1 .6 meq) reduction in serum sodium for each 5 .6 mraolfL (100 mg/dL) rise in the serum glucose]. Normal serum sodium in the setting of DKA indicates a more profound water deficit.
In “conventional” units, the calculated serum osmolality [2 X (serum sodium + serum potassium) + plasma glucose (mg/dL)/l 8 + BUN/2.8] is mildly to moderately elevated, though to a lesser degree than that found in HHS. In DKA, the ketone body, 3-hydroxybutyrate, is synthesized at a threefold greater rate than acetoacetate; however, acetoacetate is preferentially detected by a commonly used ketosis detection reagent i.e. nitroprusside.
Serum ketones are present at significant levels (usually positive at serum dilution of 1:8 or greater). The nitroprusside tablet, or stick, is often used to detect urine ketones; certain medications such as captopril or penicillamine may cause false-positive reactions.
Serum or plasma assays for (3-hydroxybutyrate more accurately reflect the true ketone body level. The metabolic derangements of DKA exist along a spectrum, beginning with mild acidosis with moderate hyperglycemia evolving into more severe findings.
Insulin shock; Low blood sugar
Hypoglycemia is a condition that occurs when your blood sugar (glucose) is too low.
Blood sugar below 70 mg/dL is considered low. Blood sugar at or below this level can harm one.
Causes, incidence, and risk factors
Hypoglycemia occurs when:
- Your body’s sugar (glucose) is used up too quickly
- Glucose is released into the bloodstream too slowly
- Too much insulin is released into the bloodstream
Insulin is a hormone that reduces blood sugar. It is produced by the pancreas in response to increased glucose levels in the blood.
Low blood sugar is most commonly seen in people with diabetes who are taking insulin or other medicines to control their diabetes.
Babies who are born to mothers with diabetes may have severe drops in blood sugar.
Hypoglycemia in people who do not have diabetes may be caused by:
- Drinking alcohol
- Insulinoma – a rare tumor in the pancreas that produces too much insulin
- Lack or deficiency of a hormone, such as cortisol or thyroid hormone
- Severe heart, kidney, or liver failure or a septicemia
- Some types of weight-loss surgery
Symptoms one may have when his/her blood sugar gets too low include:
- Double or blurry vision
- Fast or pounding heartbeat
- Feeling cranky or acting aggressive
- Feeling nervous
- Shaking or trembling
- Sleeping difficulty
- Tingling or numbness of the skin
- Tiredness or weakness
- Unclear thinking
Sometimes one’s blood sugar may be too low, even if he/she does not have symptoms. If the blood sugar gets too low, one may:
- Have a seizure
- Go into a coma
Signs and tests
Home monitoring of blood sugar with a finger stick sample will show readings lower than 70 mg/dl on your glucose monitor.