1. Critical illnesses are often associated with circulatory, respiratory, hepatic and/or renal dys­function that may alter the pharmacokinetics and/or pharmacodynamics of drugs.
2. Decisions about routes of administration and doses of drugs used during medical emergen­cies must consider the physiological status of the patient, the pharmacokinetic and pharmacodynamic characteristics of the particular drug, and how the two interact.
3. Adverse drug reactions and interactions are more likely in critically ill patients due to the effect of the disease on drug kinetics, the decreased toxic-therapeutic ratio due to severe under­lying illness, and the large number of medications that such patients receive. Adverse reactions to drugs should be considered when unexplained deterioration or failure to respond to therapy are encountered.
4. Preservation of function of vital organs is a fundamental concept of critical care therapeutics. Preservation of cardiovascular functions requires attention to fluid and electrolyte status, prompt correction of arrhythmias and shock, and measures to preserve the myocardium against ischaemic injury.
5. Preservation of respiratory function requires protection of the airway, cautious use of fluids and oxygen, and prompt recognition and management of infection.
6. Preservation of cerebral function requires maintaining cerebral blood flow with adequate oxygen and glucose sufficient to meet the metabolic demands of the brain. This entails main­taining adequate systemic circulation, control of intracranial hypertension, and prompt control of seizures and hyperthermia.



7. Critically ill patients are particularly susceptible to infections, gastric stress erosions and ulcers, adult respiratory distress syndrome, pulmonary emboli, and haemostatic disorders. The risks of such complications may be reduced by meticulous care of catheters, pulmonary toilet, cautious use of fluids, prompt treatment of infection when it occurs, and selective prophylactic drug therapies.
8. Shock can be produced by many different processes including myocardial infarction, hypovolaemia, sepsis, drug overdose, burns, hypothermia, spinal cord transsection and anaphylaxis. Optimum treatment of shock depends on knowledge of the pathophysiology of the shock state and the pharmacology of the drugs.
9. Features of acute drug intoxication include coma, agitated delirium, seizures, hypo- and hyperthermia, shock, arrhythmias, aspiration and pulmonary oedema. Successful therapy of acute drug intoxication depends on the integration and application of knowledge of the pharmacology of both the intoxicating drug and the drugs used in therapy, as well as the principles of supportive critical care.

General Information of the drug

• Miglitol works differently from other oral antidiabetes drugs, which control blood sugar levels by increasing the production of insulin or helping the body to use the hormone more efficiently.
• Miglitol delays the digestion of carbohydrates (sugars) by acting in the cells that line the small intestine, where sugar is absorbed. This results in less sugar being absorbed into the blood and therefore, a lower blood-sugar level.
• Miglitol also has some effect against the enzyme lactase, but usually does not cause lactose intolerance. Hypoglycemia (very low blood sugar) is unlikely with miglitol because of the way the drug works in diabetes.
• Miglitol may be prescribed with another antidiabetic drug if single-drug therapy is not enough to adequately control blood sugar levels.



• People taking miglitol should have their blood sugar checked periodically to see how well the drug is working. Your blood glucose should be carefully monitored if you add or withdraw any of these drugs while taking miglitol or acarbose. It is common for patients to equip themselves with Home Glucose Monitors, which is widely available.
• Thiazides and other diuretics, corticosteroid anti-inflammatory drugs, phenothiazines, thyroid drugs, estrogens, contraceptive drugs, phenytoin, nicotinic acid, stimulants, calcium channel blockers, and isoniazid may increase blood sugar levels.
• Miglitol and acarbose add to the blood-sugar-lowering effect of sulfonylureas, insulin, and other antidiabetes drugs and may increase the risk of hypoglycemia (low blood sugar) associated with these drugs.
• Miglitol may interfere with the absorption of several drugs into the blood, including propranolol, ranitidine, digoxin, glyburide, and metformin. Seek advise with your doctor as he/she may need to adjust your dose of these drugs.
• Digestive enzyme preparations, charcoal, kaolin (an ingredient in Kaopectate), and antacids—as well as other drugs intended to absorb stomach contents—reduce the effects of miglitol and acarbose. Separate dosing of these drugs by at least 2 hours.
• Combining acarbose and digoxin may increase the effects of digoxin.
• As Miglitol prevents the breakdown of table sugar, if you take Miglitol in combination with insulin or a sulfonylurea prescription drugs, make sure to have a quick source of glucose (dextrose) with you to treat hypoglycemia ( symptoms include increased hunger, tiredness, sweating, increased heart rate, and numbness in the arms and legs ).
• Take your dose with the first bite of each meal. The drug has to be present in your intestine to prevent the absorption of sugar into your blood.
• As Miglitol cannot work unless there is food in your stomach, if you do forget to take a dose of miglitol with your meal, skip the dose you forgot. At the beginning of your next meal, continue with your regular dose .
• Before buying any nonprescription drug, seek advice with your pharmacist to be sure if it is safe for diabetics to take together with acarbose.

Cautions

• Do not take miglitol if you are sensitive or allergic to any of its ingredients
• If you have diabetic ketoacidosis, cirrhosis of the liver, inflammatory bowel disease, ulcers in the colon, intestinal obstruction, absorption or digestion diseases, or if intestinal gas, it will be a severe problem. Consult your doctor before taking this prescription.
• Acarbose may lead to liver inflammation.
• People with kidney disease retain higher levels of miglitol in the blood, but this does not affect the drug’s action because it acts locally in cells lining the small intestine. For patients with severe kidney disease should not take this drug due to drug retention in the blood.

Dosage and Possible Overdose ( This Prescription is not for Child )

• Acarbose :- Adult: 25-100 mg with breakfast, lunch, and dinner.
• Miglitol :- Adult: 25-100 mg with breakfast, lunch, and dinner.
• Miglitol must be taken with the first bite of each main meal.
• Unlike other antidiabetic medicines, a miglitol overdose does not cause hypoglycemia. Overdose symptoms are likely to include gas, diarrhea, and pain.
• Follow your doctor’s instructions especially for dietary plan, exercise, and blood- sugar testing. ( See Possible Side Effects below )

Possible Side Effects
a. Acarbose
Intestinal side effects of acarbose tend to improve or go away after a few weeks.
Most common:

• stomach gas (in 75% of people who take it),
• abdominal pain,
• and diarrhea.

( These side effects may be worse if you don’t restrict the amount of carbohydrate in your diet. Consult your doctor on proper dietary plan )

Less common or Rarely Occurs :

• skin rashes.
• swelling and itching,
• hepatitis or yellowing of the skin or whites of the eyes,
• abdominal distress,
• abdominal obstruction,
• liver irritation,
• abnormalities in blood tests.

b. Miglitol ( Most side effects of miglitol go away with continued use of the drug )
Most common:  gas, diarrhea, and abdominal pain.
Less common or Rare Effects : rash and low blood iron.

** For Unusual Side Effects that you may notice, seek your doctor advise immediately !

Pregnancy/Breast-feeding period :
Nursing Mothers who must take this drug should use infant formula, as the safety of using miglitol during pregnancy is not known, but small amounts of miglitol pass into breast milk. ( Diabetes during pregnancy is usually treated with insulin. )

Seniors Adult Consumption
Seniors with severe kidney disease should avoid this medication.

*Blood levels of acarbose are higher in older adults, but this is usually not considered important. Always consult your doctor if in doubt.

This is because, unlike say sodium or glucose, the in­take of a drug is quite well known and the pro­cesses of distribution and elimination are usu­ally very simple and not under the control of a multitude of homeostatic controlling reflexes.

Given an accurate dosing history and one or more drug concentrations, it is possible to de­scribe the pharmacokinetic processes of distri­bution and elimination quite precisely in an individual patient and to make accurate predic­tions of concentrations at future points in time, whatever dosing regimen is used.

The ability to interpret drug concentrations and extract infor­mation so that future concentrations can be pre­dicted and a rational dosing scheme instituted, requires a different kind of intellectual effort from that needed to interpret, say, a serum glu­cose concentration. The latter is mostly inter­preted by reference to a so-called ‘normal range’ – usually the 95% confidence interval based upon measurements from a sample of a ‘normal’ population.

Under most circumstances, if the serum glucose concentration is within the “nor­mal range”, little further attention is paid to it If it is outside of the ‘normal range’, diagnostic efforts are made to determine what pathophys­iological process is disturbed. But the precise value will be used only in a semi quantitative fashion, eg. high, very high, or extremely high, or in reference to some previously defined diag­nostic threshold value; for example, diabetes mellitus may be diagnosed if the glucose con­centration is greater than 10 mmol/L.

On the other hand, all drug concentrations exceed the “normal” range because it would be abnormal to be able to detect any therapeutic substance in the serum of a normal, healthy individual.

The quantitative information provided by a drug concentration measurement can be use­fully applied with up to 2 significant figures in the determination of, say, drug clearance. This degree of precision is implicit in use of this in­formation because individual dosage decisions will often be made with 2 significant figures in the dose size.

The quantitative approach to therapeutic decision making is relatively new to the art of medicine. Most clinicians currently practicing medicine will not have been taught very much pharmacokinetics during their undergraduate training and may therefore have only a very hazy idea of the quantitative decisions that form the basis of rational therapeutics.

Furthermore, younger clinicians may be misled into thinking that the pharmacokinetics they were taught at medical school are irrelevant to modern medi­cine because their senior colleagues pay no at­tention to pharmacokinetic detail and make therapeutic decisions in a seemingly capricious fashion. Such a conclusion may be quite false because therapeutic decisions made by an ex­perienced clinician are founded upon a wide base of knowledge gained from treating many similar patients.

This prior knowledge of the character­istics of the population being treated provides an empirical, but nevertheless frequently satis­factory, guide to making an appropriate quan­titative and qualitative therapeutic decision. Recognition of the value of such prior infor­mation when faced with an individual patient about whom little is known is the basis of the latest techniques of rational, quantitative phar­macokinetic and pharmacodynamic forecasting.

For the person who must make a therapeutic choice on behalf of an individual patient, the application of quantitative pharmacokinetic principles can substitute for the advice of a more experienced colleague. For all clinicians, young and old, these same principles can be applied to new therapeutic entities and reduce the suf­fering of patients who would otherwise be ex­posed to the vagaries of a trial and error ap­proach.