TWELVE (12) COMMON ANTIDOTES, AND HOW THEY WORK.

An antidote is a drug or a chelating substance that counteracts the effects of another drug or a poison.

COMMON ANTIDOTES INCLUDE THE FOLLOWING:
ACETYLCYSTEINE: Has hepatoprotective effect. Used in acetaminophen (paracetamol) overdose/toxicity, thereby preventing liver damage or failure. Cysteine (an amino acid) helps in the synthesis of glutathione, an essential intracellular antioxidant, which protects the liver from free radicals and intracellular toxins. Acetylcysteine is also a mucolytic agent that loosens thick mucus secretions in patients with cystic fibrosis and chronic obstructive pulmonary disease (COPD).

ACTIVATED CHARCOAL: It is used to treat drug toxicity or poisoning. Due to its large surface area, it has the capacity to bind to toxins or poisons, thus reversing their adverse effects.

ATROPINE: It is used to treat organophosphate pesticide poisoning.

DEFEROXAMINE: Used in iron or aluminum toxicity/overdose. It chelates or binds to excess iron and aluminum, thus causing their removal from the body.

DIGIBIND: Also known as Digoxin immune fab (antigen binding fragments) or Digoxin-specific antibody. It is used to treat digoxin toxicity, hence, reversing the adverse effects of digoxin overdose.

DIMERCAPROL: For arsenic, gold, or inorganic mercury poisoning.

FLUMAZENIL: A selective benzodiazepines (diazepam, lorazepam, bromazepam, midazolam) antagonist. It is used in benzodiazepines overdose/toxicity.

GLUCAGON: Used to treat overdose or toxicity of beta-blockers (propranolol, metoprolol) and calcium channel blockers (nifedipine, nimodipine, amlodipine). It acts by directly increasing cardiac inotropy and increasing hepatic gluconeogenesis.

METHYLENE BLUE: For drug-induced methemoglobinemia.

NALOXONE: It is an opioid antagonist. It is used in opioid toxicity to reverse the adverse effects of opioid overdose by binding to opioid receptors.

PROTAMINE SULPHATE: Used to reverse the anticoagulant effect of heparin (that is, it is used in heparin overdose). It is derived from fish sperm, and it binds to heparin to form a stable salt.

VITAMIN K: Antidote for warfarin overdose/toxicity. It helps to reverse high INR (International Normalized Ratio) values in warfarin overdose.

 

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REHYDRATING A SICK CHILD

.Fluid loss, especially in children, can be fatal if prompt intervention is not taken to rehydrate the sick child. Cardinal signs that make children vulnerable to dehydration or fluid loss include: Diarrhoea, vomiting, fever, and some other disease conditions that further increase the metabolic rate in children.

Therefore, fluid and electrolyte therapy constitute a vital component of the care given to a sick child.

Fluid requirements for children are higher than those for adults for the following reasons:
1. Children have higher metabolic rates than adults. High metabolic rate is directly proportional to high caloric demand or expenditure. This translates into high fluid requirement.
2. The surface area to weight ratio is high in children. Increased surface area leads to increase insensible water loss through the skin.
3. Children have higher respiratory rates, and this equates to higher insensible losses from the respiratory tract.

ESTIMATING THE PERCENTAGE OF DEHYDRATION.
It is important to first estimate or calculate the percentage of fluid loss in children in order to know the amount of fluid deficit to be given for replacement.

METHOD 1:
IF THE PRE-ILLNESS WEIGHT OF THE SICK CHILD IS KNOWN, THE ILLNESS WEIGHT (PRESENT WEIGHT) IS MEASURED. THE DIFFERENCE BETWEEN THE PRE-ILLNESS WEIGHT AND ILLNESS WEIGHT IS DIVIDED BY THE PRE-ILLNESS WEIGHT AND THE RESULT IS MULTIPLIED BY 100.

For example:
A child weighed 10kg in the last visit to the clinic. The child was rushed to the clinic due to frequent passage of watery stool. His weight is now 9kg.

To calculate the percentage of dehydration:
(10kg – 9kg) divided by 10kg, then multiply by 100%
= (1kg divided by 10kg) times 100%
= 10%
FLUID DEFICIT = %DEHYDRATION * WEIGHT * 10
In the example given above;
Fluid deficit = 10% * 10kg * 10
= 1000ml
Therefore, the child requires 1000ml for replacement.
NOTE: The pre-illness weight is used in the formula for Fluid deficit.
THE RULE HERE IS THAT EVERY 1KG DROP IN WEIGHT REQUIRES 1L (1000ML) FLUID REPLACEMENT.

METHOD 2:
Percentage of dehydration can also be estimated through diligent clinical assessment. The signs to look out for include: Dry mucous membrane, decreases skin turgor, sunken eyes, depressed fontanels, increased thirst, low urinary output, low blood pressure, fatigue, and other signs of dehydration.

This method is applicable IF THE PRE-ILLNESS WEIGHT IS NOT KNOWN.

The nurse makes clinical judgment based on her assessment and concludes on the appropriate percentage to give to the sick child.

MILD DEHYDRATION (<3%)
Dry mucous membranes.
MODERATE DEHYDRATION (4-10%)
Dry mucous membranes, sunken eyes, decreased skin turgor, depressed fontanel.
SEVERE DEHYDRATION (>10%)
Dry mucous membranes, sunken eyes, decreased skin turgor, depressed fontanels, low urinary output, low blood pressure, delay in capillary refill time, fatigue, increased thirst.

For example:
After a diligent and careful clinical assessment of a dehydrated patient, a percentage dehydration of 12% was given. If the patient weighs 8kg, calculate the amount of fluid replacement required.

FLUID DEFICIT = %DEHYDRATION * WEIGHT * 10
= 12 * 8 * 10
= 960ml
Amount of fluid to be replaced = 960ml

NOTE:
For a sick child or hospitalized child, total fluid requirement will be the sum of MAINTENANCE FLUID AND THE DEFICIT.

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HOLLIDAY-SEGAR METHOD OF CALCULATING MAINTENANCE FLUID.

 

Fluid therapy is divided into MAINTENANCE, DEFICIT, and REPLACEMENT requirements. Our focus for this week is MAINTENANCE REQUIREMENTS.

Maintenance fluid can be defined as the amount of fluid required to compensate for ongoing fluid losses, thus maintaining steady state in the body.

It can be given by intravenous routes or oral routes (if patient can tolerate orally) or both.

Water losses in the body are classified into SENSIBLE LOSS (urine and faecal water) and INSENSIBLE LOSS (perspiration and respiration).

Holliday segar method is a widely acceptable method of calculating maintenance fluid, especially in children. It helps to estimate the fluid requirement in 24 hours. The method is based on the weight of patient in kilogram.

This formula relates water loss to the caloric expenditure. That is, for every 100 kilocalories burned, the patient utilizes 100ml.

HOLLIDAY-SEGAR METHOD:
First 10kg = 100ml per kg in 24 hrs
Second 10kg = 50ml per kg in 24hrs
Other kg (or remaining kg) = 20ml per kg in 24 hrs.

Example 1:
What will be the maintenance fluid requirement for a child weighing 6kg?

Wt= 6kg (this falls within first 10kg)
=100ml per kg
= 100ml*6 = 600ml
Therefore, the child requires 600ml of fluid in 24hrs (per day).
To express it in ml per hour, divide 600ml by 24hrs
= 25mls per hour

Example 2:
A child weighing 14kg was rushed to the emergency department. Calculate the daily maintenance fluid of the child.

Wt = 14kg (10kg + 4kg)
First 10kg = 100ml per kg
= 100ml*10= 1000ml
Second 10kg (which is 4kg) = 50ml per kg
= 50ml*4 = 200ml
Daily maintenance fluid for the child of 14kg = 1000ml + 200ml = 1200ml.

To express it in ml per hour, divide 1200ml by 24
= 50mls per hour

Example 3:
Calculate the maintenance fluid to be given to a patient weighing 22kg.

Wt = 10kg + 10kg + 2kg
First 10kg = 100ml per kg
= 100ml*10 = 1000ml
Second 10kg = 50ml per kg
= 50ml*10 = 500ml
Remaining kg (2kg) = 20ml per kg
= 20ml*2 = 40ml
Maintenance fluid = 1000ml + 500ml + 40ml
= 1540ml in 24hrs (per day).
To express it in ml per hour, divide 1540ml by 24
= 64.2ml per hour.

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ELECTROLYTES IMBALANCES ASSOCIATED WITH DIGOXIN ADMINISTRATION.

 

Electrolytes imbalances to watch out for in digoxin administration include:

HYPERKALEMIA:
Digoxin inhibits Na-K-ATPase pump on the membrane of cardiac cells. The normal activity of the Na-K-ATPase is to pump potassium into the cell and pump sodium outside the cell. This process is inhibited by digoxin, making the extracellular potassium level to rise.

HYPOKALEMIA:
If a patient is hypokalemic, this condition must be corrected before commencing digoxin therapy. In hypokalemia, digoxin easily binds to the potassium part of Na-K-ATPase (this action prevents potassium to be pumped outside the cell). Therefore, hypokalemia becomes worsened and digoxin toxicity is potentiated (since enough sites will be available for digoxin to bind).

HYPOCALCAEMIA:
Hypocalcaemia causes insensitivity to digoxin. Since digoxin performs its positive inotropic function through the influx of calcium into the cell, low calcium levels will make the drug of no effect and can also lead to its toxicity (there’s a tendency to try to increase the dose of digoxin administered to patients). Therefore, hypocalcaemia must be corrected in considering digoxin therapy.

NOTE:
Hyperkalemia in the presence of digoxin toxicity must not be treated with calcium compounds. It has been found to cause an irreversible non-contractile state called THE STONE HEART. However, if the ECG shows no p wave, 10mls of 10% calcium gluconate can be added to 100mls of dextrose in water, and allowed to run very slowly.

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EIGHT (8) IMPORTANT THINGS EVERY NURSE MUST KNOW ABOUT DIGOXIN

 

Digoxin (Lanoxin) is a cardiac glycoside. It is also called DIGITALIS because it is derived from a plant named DIGITALIS LANATA.

8 THINGS EVERY NURSE MUST KNOW ABOUT DIGOXIN.

DIGOXIN HAS A POSITIVE INOTROPIC EFFECT.
It increases the force of myocardial contractility. This makes it useful in the treatment of congestive heart failure.

DIGOXIN HAS A NEGATIVE CHRONOTROPIC EFFECT.
It slows down the rate of cardiac contraction (this is the rationale for counting patient’s pulse before administering digoxin), thus strengthening the heart muscles to effectively pump blood. This makes it useful in atrial fibrillation. Th

DIGOXIN HAS A NARROW THERAPEUTIC INDEX.
Therapeutic index is the ratio between the dosage of a drug that causes a lethal/toxic effect and the dosage that causes a therapeutic effect. Because of its narrow therapeutic index, toxicity may result even with mildly increased digoxin level. The normal serum digoxin level ranges between 0.5-1.5ng/ml. If digoxin level in the blood exceeds 2ng/ml, digoxin toxicity (a life-threatening condition) has already set in.

DIGIBIND IS THE ANTIDOTE FOR DIGOXIN TOXICITY.
Digibind is a digoxin-specific antibody or digoxin immune antigen-binding fragments (Fab) that is used to treat digoxin overdose or digoxin toxicity.

DIGOXIN HAS A LONG HALF-LIFE.
The half-life of a drug is the time taken for the drug’s concentration to be reduced by half in the blood. The half-life of digoxin in a patient with normal renal function is between 36-48hrs. This value will definitely increase in patients with renal impairment, since digoxin is eliminated primarily through the kidneys. Because of the long half-life of digoxin, if toxicity occurs, it takes a long time achieve a therapeutic serum digoxin level. It also takes a long time to achieve a therapeutic serum digoxin level in patients who is just starting the medication.

DIGOXIN TOXICITY IS BEST IDENTIFIED AFTER 6HOURS OF DIGOXIN ADMINISTRATION.
There’s an initial rise in the serum digoxin level earlier than 6hours of its administration. A steady state is achieved after 6hours of administration.

DIGITALIZATION.
This is the process of administering loading doses of digoxin to patients in order to achieve/attain a therapeutic plasma concentration of digoxin. After which patient continues with the maintenance dose.

LOADING DOSE AND MAINTENANCE DOSE OF DIGOXIN.
Loading dose of digoxin: 0.5-0.75mg (2 doses, at least 6hrs apart) for digitalization.
Maintenance dose: 0.125-0.25mg daily.

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INTENSIVE INSULIN THERAPY

This is also known as BASAL-BOLUS INSULIN THERAPY.

Naturally, in a non-diabetic person, the body helps to regulate the blood glucose level by releasing basal and bolus insulin.

Basal insulin is the background insulin that is normally produced by the beta cells of the pancreas during periods of fasting (between meals and during sleep). It is present/sustained in the body 24 hours in a day whether the person eats or not.

Bolus insulin is the extra amounts of insulin produced immediately after meal, in response to the rise in glucose level in the blood. The amount of insulin produced here depends on the calories contained in the food taken in.

Basal-bolus insulin therapy mimics this same mechanism to control the blood glucose level.

Basal insulin therapy uses intermediate insulin (NPH, Novolin N, Humulin N) and long-acting insulin (Lantus and Levemir) to mimic the normal physiology of the body. Intermediate insulin takes 2hrs to start work and lasts for 12-18hrs. Long-acting insulin takes 2hrs to start work and lasts for 20-24hrs. These characteristics make them suitable to be used as basal insulin. They are usually given at bedtime and/or before breakfast. And they work round the clock.

Bolus insulin therapy uses rapid-acting insulin (Novolog, Humalog and Apidra) and short-acting or regular insulin (Novolin R, Humulin R) to mimic the normal physiology of regulation of blood glucose level.
Rapid-acting insulin takes just 15minutes to start work and lasts for about 3hours in the blood. Short-acting insulin takes 30minutes to start work and lasts for about 8hrs. They are usually given 15-30minĀ  pre-meal (pre-prandial) to help lower the rise in blood sugar at meal time. And some times it may be given immediately before or after meal.

If insulin pump is used, low dose of rapid-acting/short-acting insulin is set in the pump to be delivered at a constant rate – this acts as the BASAL INSULIN. Then at meal time, a higher dose is given – this acts as the BOLUS INSULIN. Therefore, in this case, rapid/short acting insulin serve as both basal and bolus insulin.

NOTE:
Lantus is usually given at bed time. This is because if it’s action fades away before 24 hours, it will be during the day, which is safer. Also, lantus must be administered at the same time every day.

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CALCIUM GLUCONATE AND MASSIVE BLOOD TRANSFUSION

CALCIUM GLUCONATE AND MASSIVE BLOOD TRANSFUSION (MBT).

Massive blood transfusion (MBT) is arbitrarily defined as the replacement of a patient’s total blood volume in less than 24 hours, or as the acute administration of more than half the patient’s estimated blood volume per hour.

One of the major complications of MASSIVE BLOOD TRANSFUSION is HYPOCALCEMIA.

Each unit of blood contains approximately 3g of citrate (the anticoagulant in the blood bag that helps to prevent clotting of stored blood and blood products). Citrate chelates (binds to) ionic calcium to form a complex thus reducing the calcium level in the blood, a condition referred to as HYPOCALCEMIA.

The normal adult liver metabolizes 3g of citrate every 5 minute. This helps to clear up citrate from the blood. But in critically ill patients and in patients with impaired or compromised liver function, citrate accumulates in the body, causing citrate toxicity and hypocalcaemia. Hypothermia is another factor that can reduce the rate at which citrate is metabolized from the body.

Calcium is an important co-factor, especially in coagulation, and has a key role in mediating the contractility of myocardial, skeletal and smooth muscles. Hypocalcaemia results in hypotension, small pulse pressure, flat ST-segments and prolonged QT intervals on the ECG.

If there is clinical, biochemical or ECG evidence of hypocalcaemia, it should be treated with 5-10ml intravenous injection of calcium gluconate 10% given slowly over 3-5min.

Normal range of calcium in the blood: 8.5-10.5 mg/dl

 

NOTE:
To convert mmol/L to mg/dl, multiply by 18.
To convert from mg/dl to mmol/L, divide by 18.

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