Posted in General Medicine for OMFS

Fluid and Electrolyte Balance Physiology

FLUID AND  ELECTROLYTE BALANCE PHYSIOLOGY

Introduction:

Cell function depends not only on a continuous supply of nutrients and removal of metabolic wastes, but also on the physical and chemical homeostasis of the surrounding fluids.

Body Fluids

Body water content

In a healthy young adult, water probably accounts for about half body weight (mass). However not all bodies contain the same amount of water, and total body water is a function not only of weight, age and sex but also of the relative amount of body fat. Because of their low body fat and low bone mass, infants are 73% or more water.

But total water content declines throughout life, accounting for only about 45% of body weight in old age. A healthy young woman about 50%. This significant difference between the sexes reflects the relatively larger amount of body fat and smaller amount of skeletal muscle in females. Of all body tissues, adipose tissue is least hydrated containing up to 20% water; even bone contains more water than does fat. By contrast, skeletal muscle is about 65% water. Thus, people with greater muscle mass have proportionately more body water.

 Fluid compartments

Water occupies two main fluid compartments within the body. A little less than two-thirds by volume is in the intracellular fluid (ICF) compartment, which actually consists of trillions of tiny individual compartments: the cells. In an adult male of average size (70kg). ICF accounts for about 25L of the 40L of body water. The remaining one-third or so of body water is outside cells, in the extracellular fluid (ECF) compartment. The ECF compartment is, in turn, divisible into two important subcompartments: (1) plasma, the fluid portion of blood within the blood vessels and (2) interstitial fluid (IF), the fluid in the microscopic spaces between tissue cells. Additionally, there are numerous other examples of ECF that are distinct from both plasma and interstitial fluid such as lymph, cerebrospinal fluid, and secretions of the gastrointestinal tract.

In the 70kg adult male, interstitial fluid accounts for approximately 12L and plasma about 3L of total (15L)ECF volume.

Composition of Body Fluids

Solutes: Electrolytes and Nonelectolytes

Water serves as the universal solvent in which a variety of solutes are dissolved. Solutes may be classified broadly as electrolytes and nonelectrolytes. The non electrolytes have bonds that prevent them from dissociating in solution; therefore, they have no electrical charge. Most nonelectrolytes are organic molecules – glucose, lipids, creatinine and urea. In contrast, electrolytes are chemical components that do dissociate into ions in water. Because ions are charged particles, they can conduct an electrical current – hence the name electrolyte. Typically, electrolytes include inorganic salts, both inorganic and organic acids and bases, and some proteins.

Although all dissolved solutes contribute to the osmotic activity of a fluid, electrolytes have much greater osmotic power than nonelectrolytes because each electrolyte molecule dissociates into at least two ions. For example, a molecule of sodium chloride (NaCl) contributes twice as many solute particles as glucose (which remains undissociated), and a molecule of magnesium chloride (MgCl2) contributes three times as many:

NaCl à Na+ + Cl                    (two particles)

MgCl2 à Mg2+ + Cl + Cl–         (three particles)

Glucose à glucose                           (one particle)

Regardless of the type of solute particle, water moves according to osmotic gradients – from areas of lesser osmolality to those of greater osmolality. Thus, electrolytes have the greatest ability to cause fluid shifts.

Electrolyte concentrations of body fluids are usually expressed in milliequivalents per liter (mEq/L), a measure of the number of electrical charges in 1 liter of solution. Because the total number of negative charges (anions) in a solution is always equal to the number of positive charges (cations), the milliequivalent system of reporting electrolyte concentrations makes it easier to follow electrolyte shifts.

The concentration of any ion in solution in mEq/L can be computed using the equation.

Concentration of ion (mg/L)

mEq/L =                                                          x  No. of electrical charges on one ion

atomic weight of ion

 

Comparison of Extracellular and Intracellular Fluids

Each fluid compartment has distintictive pattern of electrolytes. But except for the relatively high protein content in plasma, the extracellular fluids are very similar. Their chief caution is sodium, and their major anion is chloride. However, plasma contains somewhat fewer chloride ions than interstitial fluid, because the nonpenetrating plasma proteins are normally anions and plasma is electrically neutral.

In contrast to extracellular fluids, intracellular fluid contains only small amounts of Na+ and Cl. Its most abundant cation is potassium, and its major anion is phosphate (HPO42-). Cells also contain moderate amounts of magnesium ions and substantial quantities of soluble proteins (about three times the amount found in plasma).

Sodium and potassium ion concentrations in extracellular and intracellular fluids are nearly opposite. The characteristic distribution of these ions on the two sides of cellular membranes reflects the activity of cellular ATP-dependent sodium-potassium pumps, which keep intracellular Na’ concentrations low while maintaining high intracellular K+ concentrations.

Fluid Movement Among Compartments

The continuous exchange and mixing of body fluids are regulated by osmotic and/or hydrostatic pressures. Although water moves freely between the compartments along osmotic gradients, solutes are unequally distributed because of their molecular size, electrical charge, or dependence on active transport.

Exchanges between plasma and interstitial fluid occur across capillary membranes.

Nearly protein-free plasma is forced out of the blood stream into the interstitial space by the hydrostatic pressure of blood. This filtered fluid is almost completely reabsorbed into the bloodstream in response to the colloid osmotic (oncotic) pressure of plasma proteins. Under normal circumstances, the small net leakage that remains behind in the interstitial space is picked up by lymphatic vessels and returned to the bloodstream.

Exchanges between the interstitial and intracellular fluids are more complex because of the selective permeability of cellular membranes. As a general rule, two-way osmotic flows of water are substantial. But ion fluxes are restricted and, in most cases, ions move selectively by active transport. Movements of nutrients, respiratory gases, and wastes are typically unidirectional. For example, glucose and oxygen move into the cells and metabolic wastes move out of the cells and into the blood.

Of the various body fluids, only plasma circulates throughout the body and serves as the link between the external and internal environments. Exchanges occur almost continuously I the lungs, gastrointestinal tract, and kidneys. Although these exchanges alter plasma composition and volume, they are quickly followed by compensating adjustments in the other two fluid compartments so that balance is restored.

Many factors can cause marked changes in ECF and ICF volumes. However, water moves freely between compartments, so the osmolalities of all body fluids are equal, except for the first few minutes after a change in one of the fluids occurs. Increasing the solute content of the ECF (most importantly, the NaCl concentration) can be expected to cause osmotic changes in the ICF-namely, a shift of water out of the cells. Conversely, decreasing the osmolality of the ECF causes water to move into the cells. Thus, the volume of the ICF is determined by the solute concentration of the, ECF.

WATER BALANCE

To remain properly hydrated, water intake must be equal water output Water intake varies Widely from person to person and is strongly influenced by habit, but it is typically about 2500 ml a day in adults. Most water enters the body through ingested liquids (about 60%) and solid foods (about 30%). About 10% of body water is produced by cellular metabolism; this is Called metabolic water or water of oxidation.

Water output occurs by several routes. Some water (28%) vaporizes out of the lungs in expired air or diffuses directly through the skin; this is called insensible water loss. Some, is lost in obvious perspiration (8%) and in feces (4%). The balance (60%) is excreted by the kidneys in urine.


Regulation of Water Intake:

The Thirst Mechanisms

Thirst is the driving force for water intake, but the thirst mechanism is poorly understood It appears    that a decrease in plasma volume of 10% (or more, as from hemorrhage) and / or an increase in plasma- osmolality of 1% to 21% results in a dry mouth and excites the hypothalamic thirst center. A dry mouth occurs because the rise in plasma oncotic pressure causes less fluid to leave the bloodstream. Because the salivary glands obtain the water they require from the blood, less saliva is produced. The hypothalamic          thirst center, is stimulated when its osmoreceptors     lose water by osmosis  to the hyportonic ECF, an event that causes them to become irritable and depolarize. Collectively, these events cause a subjective sensation of thirst, which motivates us to get a drink. This mechanism helps explain the nagging thirst of a hemorrhaging  patient who has lost 800ml or more of blood.

Regulation of Water Output

Output of certain amounts of water are unavoidable. Obligatory water losses include insensible water losses from the lungs and through the skin, water that accompanies undigested food residues in feces, and a minimum daily sensible water loss of 500ml in urine. Obligatory water loss in urine reflects the facts that (1) when we eat an adequate diet, our kidneys must excrete about 900 – 1200 mosm of solutes to maintain blood homeostasis, and (2) human kidneys must flush urine solutes out of the body in water.

Beyond obligatory water loss, the solute concentration and volume of urine excreted depend on fluid intake, diet, and water loss via other avenues. Normally, the kidneys begin to eliminate excess water about 30  minutes after it is ingested. This delay mainly reflects the time required for ADH release to be inhibited. Diuresis reaches a peak in 1 hour and then declines to its lowest level after 3 hours.

The body’s water volume is closely tied to a powerful water “magnet,” ionic sodium.

Disorders of Water Balance

The principal abnormalities of water balance are dehydration, hypotonic hydration, and edema, and each of these conditions offers a special set of problems to its victims.

Dehydration

Dehydration occurs when water loss exceeds water intake over a period of time and the body is in negative fluid balance. Dehydration is a common sequel to hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, and diuretic abuse. Dehydration may also be caused by endocrine disturbances, such as diabetes mellitus or diabetes insipidus.

Early signs and symptoms of dehydration include a “cottony” or sticky oral mucosa, thirst, dry flushed skin, and decreased urine output. If prolonged, dehydration may lead to weight loss, fever, and mental confusion. Another very serious consequences of water loss from the plasma ECF compartment is inadequate blood volume to maintain normal circulation and ensuing hypovolemic shock.

In all these situations, water is lost from the ECF. This is followed by the osmotic movement of water from the cells into the ECF, which equalizes the osmolality of the extracellular and intracellular fluids even though the total fluid volume has been reduced. Though the overall effect is called dehydration, it rarely involves only a deficit of water. Most often, as water is lost electrolytes are lost as well.

Hypotonic Hydration

When the osmolality of the ECF starts to drop (usually this reflects a deficit of Na+), several compensatory mechanisms are set into motion. Once of these is inhibition of ADH release, and as a result, excess water is quickly flushed from the body in urine. But when there is renal insufficiency or an extraordinary amount of water is drunk very quickly, a type of cellular overhydration called hypotonic hydration or water intoxication may result. In either case, the ECF is diluted – its sodium content is normal, but excess water is present.

This in turn promotes net osmosis into the tissue cells, causing them to swell as they become abnormally hydrated.

The resulting electrolyte dilution leads to severe metabolic disturbances evidenced by nausea, vomiting, muscular cramping, and cerebral edema. Water intoxication is particularly damaging to neurons. Uncorrected cerebral edema quickly leads to disorientation, convulsions,  coma, and death.

Edema

Edema is an atypical accumulation of fluid in the interstitial space, leading to tissue swelling. Edema may be caused by any event that steps up the flow of fluid out of the bloodstream or hinders its return.

Factors that accelerate fluid loss from the bloodstream include increased blood pressure and / or capillary permeability. Increased blood pressure can result from incompetent venous valves, localized blood vessel blockage, congestive heart failure, hypertension, or high blood volume, for instance, during pregnancy or resulting from abnormal retention of sodium.

Increased capillary permeability is usually due to an ongoing inflammatory response. Inflammatory chemicals cause local capillaries to become very porous, allowing large amounts of exudates to form.

Edema caused by hindered fluid return to the bloodstream usually reflects an imbalance in the colloid osmotic pressures on the two sides of the capillary membranes. For example,  hypoproteinemia.

ELECTROLYTE BALANCE

Electrolytes include salts, acids, and bases, but the term electrolyte balance usually refers to the salt balance in the body. Salts provide minerals essential for neuromuscular excitability, secretory activity, membrane permeability, and many other cellular functions. Additionally, salts are important in controlling fluid movements.

Salts enter the body in foods and fluids, and small amounts are generated during metabolic activity. Salts are lost from the body in perspiration, feces, and urine.

The Central Role of Sodium in Fluid and Electrolyte Balance

Sodium holds a pivotal position in fluid and electrolyte balance and overall body homeostasis, and regulating the balance between sodium input and output is one of the most important functions of the kidneys.

Sodium is the single most abundant cation in the ECF and is the only one exerting significant osmotic pressure. Additionally, cellular plasma membranes are relatively impermeable to Na+, but some does manage to diffuse in and must be pumped out against its electrochemical gradient. These two qualities give sodium the primary role in controlling ECF volume and water distribution in the body.

It is important to understand that while the sodium content of the body may change, its concentration in the ECF normally remains stable because of immediate adjustments in water volume.

Regulation of Sodium Balance

Influence and Regulation of Aldosterone

When aldosterone concentrations are high, virtually all the remaining Na’ (actually NaCl, because Cl- is cotransported) is actively reabsorbed in the distal convoluted tubules and collecting ducts. Water follow if it can, that is, if the tubule permeability has been increased by ADH.

However, when aldosterone release is inhibited, virtually no Na’ reabsorption occurs beyond the distal tubule.

Aldosterone is produced by adrenal cortical cells. The most important trigger for aldosterone release is the rennin-angiotensin mechanism mediated by the juxtaglomerular apparatus of the renal tubules.

Cardiovascular System Baroreceptors

Blood volume is carefully monitored and regulated to maintain blood pressure and cardiovascular function. As blood volume (hence pressure) rises, baroreceptors in the heart and in the large vessels of the neck and thorax (carotid arteries ad aorta) alert the hypothalamus. Shortly after, sympathetic nervous system impulses to the kidneys decline, allowing the afferent arterioles to dilate. As the glomerular filtration rate rises, sodium and water output increase. This phenomenon, called pressure diuresis, reduces blood volume and consequently, blood pressure. In contrast, drops in systemic blood pressure lead to constriction of the afferent anterioles, which reduces filtrate formation and urinary output and increases systemic blood pressure.

Influence and Regulation of ADH

The amount of water reabsorbed in the collecting ducts of the kidneys is proportional to ADH release. When ADH levels are low, most of the water reaching the collecting ducts is simply allowed to pass through. The result in dilute urine and a reduced volume of body fluids. When ADH levels are high nearly all of the filtered water is reabsorbed and a small volume of highly concentrated urine is excreted.

Osmoreceptors of the hypothalamus sense the ECF solute concentration and trigger or inhibit ADH release from the posterior pituitary accordingly. A decrease in sodium ion concentration inhibits ADH release and allows more water to be excreted in urine, restoring normal Na’ levels in the blood. An increase in sodium levels stimulates ADH release both directly by stimulating the hypothalamic osmoreceptors and indirectly via the rennin-angiotensin mechanism. Factors that specifically trigger ADH release by reducing blood volume include prolonged fever; excessive sweating, vomiting, or diarrhea; severe blood loss; and traumatic burns.

Influence and Regulation of Atrial Natriuretic Peptide

It reduces blood pressure and blood volume by inhibiting nearly all events that promote vasoconstriction and Na+ and water retention. A trial natriuetic peptide is a hormone that is released by certain cells of the heart atria when they are stretched by the effects of elevated blood pressure.

Influence of Other Hormones

Female Sex Hormones – The estrogens are chemically similar to aldosterone and, like aldosterone, they enhance NaCl reabsorption by the renal tubules.

Progesterone seems to decrease sodium reabsorption by blocking the effect of aldosterone on the renal tubules. Thus, progesterone has a diuretic like effect and promotes sodium and water loss.

Glucocorticoids – The usual effect of glucocorticoids, such as cortisol and hydrocortisol, is to enhance tubular reabsorption of sodium. i.e. Promote edema.

Regulation of Potassium Balance

Potassium the chief intracellular cation, is required for normal neuromuscular functioning as well as for several essential metabolic activities, including protein synthesis.

Potassium excess in the ECF decrease their membrane potential, causing depolarization, which is often followed by reduced excitability. A deficit of K+ in the ECF causes hyperpolarization and nonresponsiveness. The heart is particularly sensitive to K+ levels. Both too much too little K+ (hyperkalemia and hypokalemia respectively) can disrupt electrical conduction in the heart, leading to sudden death.

Regulatory Site: The Cortical Collecting Duct

Like sodium balance, potassium balance is maintained chiefly by renal mechanisms.

The renal tubules predictably reabsorb over 90% of the filtered K+, leaving less than 10% to be lost in urine regardless of need. The responsibility for K+ balance falls chiefly on the cortical collecting ducts, and is accomplished mainly by changing the amount of potassium secreted into the filtrate.

Essentially, two factors determine the rate and extent of potassium secretion – the plasma potassium ion concentration and aldosterone levels.

Influence of Plasma Potassium Concentration

The single most important factor influencing potassium secretion is the K+ concentration in blood plasma. A high-potassium diet increases the K+ into the principal cells of the collecting duct and prompts them to secret K+ into the filtrate so that more potassium is excreted. Conversely, a low-potassium diet or accelerated K+ loss depresses its secretion by the collecting ducts.

Influence of Aldosterone

As aldosterone stimulates the principal cells to reabsorb sodium, it simultaneously enhances potassium ion secretion.

To maintain electrolyte balance there is a one-for-one exchange of Na+ and K+ in the cortical collecting ducts. For each Na+ reabsorbed, a K’ is secreted. Thus, as plasma Na+ level rise, K’ levels fall proportionately.

Adrenal cortical cells are directly sensitive to the K+ content of the ECF bathing them. When it increases even slightly, the adrenal cortex is strongly stimulated to release adlosterone, which increases potassium secretion.

Regulation of Calcium Balance

About 99% of the body’s calcium is found in bones in the form of calcium phosphate salts, which provide strength and rigidity to the skeleton. Ionic calcium in the ECF is important for normal blood clotting, cell membrane permeability, and secretory behavior. Like sodium and potassium, ionic calcium has potent effects on neuromuscular excitability. Hypocalcemia increases excitability and causes muscle tetany. Hypercalcemia is equally dangerous because it inhibits neurons and muscle cells and may cause life-threatening cardiac arrhythmias.

Calcium balance is regulated primarily by the interaction of two hormones – parathyroid hormone and calcitonin.

Influence of Parathyroid Hormone

The most important controls of Ca2+ homeostasis are exerted by parathyroid hormone (PTH), released by the tiny parathyroid glands located o the posterior aspect of the thyroid gland in the pharynx. Declining plasma levels of Ca2+ directly stimulate the parathyroid glands to release PTH, which promotes an increase in calcium levels by targeting the following organs.

  1. Bones – PTH activates osteoclasts (bone-digesting cells), which break down the bone matrix, resulting in the release of Ca2+ and PO42– to the blood.
  2. Small intestine – PTH enhances intestinal absorption of Ca2+ indirectly by stimulating the kidneys to transform vitamin D to its active form, which is a necessary cofactor for calcium absorption by the small intestine.
  3. Kidneys – PTH increases calcium reabsorption by the renal tubules while simultaneously decreasing phosphate ion (PO42–) reabsorption.

When calcium levels in the ECF are within normal limits (9-11mg/100ml blood) or are high, PTH secretion is inhibited. Consequently, release of calcium from bone is inhibited, larger amounts of calcium are lost in feces and urine, and more phosphate is retained.

Influence of Calcitonin

Calcitonin, a hormone produced by the parafollicular cells of the thyroid gland, is released in response to rising blood calcium levels. Calcitonin targets bone, where it encourages deposit of calcium salts and inhibits bone reabsorption.

Regulation of Magnesium Balance

Magnesium, the second most abundant intracellular cation, activates the coenzymes needed for carbohydrate and protein metabolism and plays an essential role in myocardial functioning, neurotransmission, and neuromuscular activity. Half of the magnesium in the body is in the skeleton. Most of the remainder is found intracellularly.

Control of magnesium balance is poorly understood, but a renal transport maximum for magnesium is known to exist.

Regulation of Anions

Chloride is the major anion accompanying sodium in the ECF and, like sodium, it helps maintain the osmotic pressure of the blood. When blood pH is within normal limits or is slightly alkaline, about 99% of filtered chloride ions are reabsorbed. In the PCT, they move passively and simply follow sodium ions out of the filtrate and into the peritubular capillary blood.

Most other anions, such as sulfates and nitrates, have definite transport maximums and when their concentrations in the filtrate exceed their renal thresholds, excesses still over into urine.

 

 

References

  • Human Anatomy & Physiology – Marieb.
  • Human Anatomy & Physiology – Von De Groaf Fox.
  • Fundamental of Anatomy and Physiology – Martini.
  • Textbook of Medical Physiology – Guyton.
  • Text book of Concise Medical Physiology – Choudhary.
  • Principles of Internal Medicine – Harrison’s.
  • Principles and Practice of Medicine – Davidson.

 

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Posted in General Medicine for OMFS

Principles Of Antibiotics In Maxillofacial Surgery

Introduction

Beginning with the early work of Sir Alexander Flemming in 1929, when penicillin became the first “miracle drug”, innumerable lives been saved from such scourges as pneumonia, wound sepsis and bacterimia. Dentists benefited greatly from the discovery of penicillin, because of most odontogenic infections are caused by penicillin sensitive microorganisms.

These are the substances produced by microorganisms which suppress the growth of or kill the other microorganisms at very low concentrations.

Classification:

  1. A) Chemical structure:
  • Sulphonamides and related drugs – Sulfadiazine and others.

Sulfones – Dapsone (DDS), Para aminosalicylic acid (PAS).

  • Diaminopyrimidines – Trimethoprim, pyrimethamine.
  • B-lactam antibiotics – Penicillins, cephalosporins, monobacteriums, carbapenams.
  • Tetracyclines : Oxytetracycline, doxytetracycline etc.
  • Nitrobenzene derivatives: Chloramphenicol.
  • Aminoglycosides: Streptomycin, gentamycin, neomycin etc.
  • Macrolide: Erythromycin, oleandomycin, roxithromycin.
  • Nitrofuran derivatives: Nitrofurantoin, furazolidone.
  • Nitroimidazoles: Metronidazole, Tinidazole.
  • Quinolones: Nalidixic acid, norfloxacin, ciprofloxacin.
  • Nicotinic acid derivatives – Isoniazid, pyrizinamide, ethionamide.
  • Polyene antibiotics – Nystatin, amphotericin-B Hamycin.
  • Imidazole derivatives: Miconazole, ketoconazole, clotrimazole.
  • Others Rifampin, clindamycin, spectinomycin, vancomycin, lincomycin, sodium fluridate, cycloserine, viomycin, ethambutol, thiacetazone, clofazimine, griseofulvin.
  1. B) Mechanism of Action:
    1. Cell wall action – penicillin, caphalosporins, vancomycin.
    2. Protein synthesis interference – Erythromycin, chloramphenicol tetracycline.
    3. Detergent effect – Polymyxin, nystatin, amphotericin.
    4. Nucleic acid metabolism interference – Ciprofloxacin metronidazole.
    5. Intermediary metabolism – Trimethoprim, sulfonamides.
    6. C) Spectrum of activity:

Narrow spectrum – penicillin G, streptomycin and erythromycin.

Broad spectrum – Tetracyclines, chloramphenicol.

Extended spectrum – Penicillins, new cephalosporins, aminoglycoside.

  1. D) Type of organisms against which:
  1. Antibacterial – Penicillin, Aminoglycosides, erythromycin etc.
  2. Antifungal – Griseofulvin, amphotericin-B, Ketoconazole etc.
  3. Antiviral – Idoxuridine, acyclvir, amantadine, zidovudine etc.
  4. Antiprotozoal – Chloroquine, pyrimethamine, metronidazole, diloxanide etc.
  5. Antihelminthic – Mebendazole, piperazine, pyrantel, niclosamide etc.
  6. E) Type of action:

Bacteriostatic – Sulfonamides, tetracyclines, Chloromphenicol, Erythromycin, ethambutol.

Bactericidal – Penicillins, polypeptides, rifampin aminoglycosides, cotrimaxozole, cephalosporins, vancomycin, nalidixic acid, ciprofloxacin, isoniazid.

Some primarily static drugs may become cidal at higher concentrations.

  1. F) Source:

Fungi- Penicillin, cephalosporin, Griseofulvin.

Bacteria – Polymyxin B, Colistin, Bacitran, Tyrothricin Aztreonam.

Actinomycetes – Aminoglycosides, tetracyclines, chloramphenicol macrolides, polyenes.

Antibiotics useful for orofacial infections:

  • Penicillins
  • Clindamycin and Lincomycin.
  • Newer beta-lactum antibiotics
  • Carbapenems
  • Monobactams
  • Fluoro quinolones – ciprofloxacin.
  • Sulfonamides and trimethoprim.


Penicillins

Discovered in 1929, it was first antibiotic drug to be used.

Classification:

  1. Naturally occurring penicillins – penicillin G (t ½ 0.5hr), phenoxymethyl penicillin v. (t½ – 1hr) (0.1-3.0) MIC.
  2. Semisynthetic penicillins:
  3. Short acting – ampicillin (t ½ 0.7hr), amoxicillin, (1.0hr), amoxicillin with clavulanic acid, piperacillin and methicillin. They are stable to gastric acids and resistant to beta lactamase.
  4. Long acting – Procaine penicillin, procaine penicillin fortified and benzathine penicillin.

Penicillin is linked with procaine to provide a sustained release preparation which gives an effective level of penicillins over a period of 24 hours.

Route of administration:

Oral route is the safest and most frequently employed.

Broad spectrum I.V. administration. The spectrum of bacterial activity is much greater following IV use of penicillins because of higher serum levels achieved. The semisynthetic penicillins are well absorbed following oral administration.

Amoxycillin – Well absorbed orally.

Under GA or sedation or where atropine is used parental route should be employed.

Antibiotics should be continued for 4 to 5 days to prevent reinfection/ recurrence and to completely eradicate the disease.

Broad spectrum effect with clavulanic acid:

Clavulanic acid is derived from streptomycetclavuligerous. It acts by inhibiting beta lactamase enzymes. The result of combining with amoxicillin is to broaden antibacterial spectrum of amoxicillins to include organisms that are resistant to amoxicillin because of betalactamase production. Ex. Species of staphylococci, non-haemolytic streptococci (including strep faecalis) and some gram-ve bacteria like haemophilus, E.coli, klebsiela and proteus.

Adverse effects:

Hypersensitivity:

Anaphylaxis – Sudden onset, coughing, tonic spasms grasping, cyanosis, weak pulse and rapid drop in BP.

Allergy – Skin rashes, dermatitis, serum sickness, alteration of the efficacy of oral contraceptives.

Mechanism of action: Penicillin acts by interference of cell wall synthesis when bacteria divide in the presence of a beta-lactam antibiotics cell wall deficient forms are produced because the interior of bacterium is hyperosmotic, the CWD forms swell and burst leading to bacterial lysis.

Cephalosporins:

Similar structure to penicillin but have a difference source. Bactericidal MIC 2.8-8,

Indications:

Gram positive cocci (enterococci) and most staphylococci.

Alternate to penicillins.

Classification:

Ist Generation against gram positive

Gram +ve cocci except enterococci methicillin resistant staph aureus and straph epidermidis. Ecoli, Klebsilla, pneumonia and P.mirabilis.

Includes : Cephalothin ( t ½ 0.5) and cephalexin (t ½ 1.8hrs) cefazolin.

IInd  Generation of greater activity against gram +ve organisms to first generation cephalosporins includes cofaclor, cefuroxime.

IIIrd generation less activity against gram +ve than I generation drugs. More activity against enterobacteriacae including beta lactamase producing strains ceftriaxone, cefoperazone, cefotaxime.

Erythromycin: t ½ – 1.5 hrs; MIC 0.1-1:

Macrolide group of antibiotics. Bacteriostatic other macrolides are azithromycin and roxithromycin. Effective against – Gram +ve cocci including many penicillin resistant strains of staphylococcus and staph aureus, and many gram –ve bacteria in dental infections.

It is bacteriocidal in few circumferences.

It should be administered one hour before meal coz food may alter the absorption.

It is excreted unchanged via liver and partly kidneys.

Mechanism of action:

Acts by inhibiting protein synthesis. Combines with ribosomes and interferes with translocation. It suppresses the synthesis of larger proteins.

Toxic effects – Allergy – rare anaphyllaxis.

Nausea, vomiting, diarrhoea etc.

Cholestatic hepatitis – related to the use of estolate forms.

Interactions:

  1. With antihistamines and sympathomimetics. When used in conjunction with astemizole leads to increased levels of astemizole leading to serious arythmias. When used with terfenadine – potential for arythemias.
  2. With theophyline – Erythromycin when given in high concentrations of theophylline may produce theophylline toxicity including arythmias.
  • With carbamazapine – carbamazapine toxicity.
  1. With warfarin – increased prothrombin time and increased risk of bleeding.
  2. With benzodiazepines – increases the half life of benzodiazepines (midazolam and triazolam).
  3. With oral contraceptives – Alters the actions.

They are less effective when used with penicillins and cephalosporins, lincomycin and clindamycin should not be used along with erythromycin.

  1. Lincomycin and clindamycin (t ½ 2.7 hr) MIC 0.1-3.1:

Lincomycin is reserved for parenteral administration and clindamycin is more active and has less side effects as for oral administrations. They are bacteriostatic acting by inhibiting protein synthesis. They are effective against most gram+ve and many gram-ve bacteria including bacteriodes, anaerobic streptococci and clostridia.

They are very effective in bone infections and form a second line of treatment is osteomyelitis.

Mechanism of action – Similar to erythromycin i.e. inhibits protein synthesis by binding to ribosomes and interferes the translocation.

Toxic effects: Nausea, vomiting, diarrhea, candidaisis may occur and neither antibiotic may be used in presence of candida infections.

Neutropenia, leucopenia, agranulocytosis and thrombocytopenic purpura, pseudomembraneous colitis characterized by diarrhea, abdominal pain, fever and blood and mucus faeces.

  1. Metronidazole (t ½ 4.0hr) MIC<3.0:

Effective in anaerobic infections and ANUG. It is used with one of the penicillins to treat orofacial infections. It can also be used with cephalosporins in penicillin allergic patients.

It is effective against gram +ve and –ve bacteria including bacteriodes, clostridia and spirochetes.

It is absorbed from GIT and competes with food. It is excreted in urine which may be coloured red brown. Impaired renal and hepatic function can prolong presence of drug in serum. Also excreted in saliva and breast milk in similar concentration to plasma.

Toxic effects:

Teratogenic effects are possible:

Blood dyscrasias, if therapy exceed ten days. It will affect patients with CNS pathology such as depression or psychosis.

Convulsions, dizziness, vestibular symptoms, hypotension and hallucinations.

It is contraindicated in patients taking phenytoin. It may enhance the effects of warfarin and prolong coagulation time.

Mechanism of action : It enters the microorganisms by diffusion, gets reduced to intermediate compounds which causes cytotoxicity by damaging DNA. It also inhibit cell mediated immunity to induce mutagenesis and cause radiosensitization.

  1. Aminoglycosides: MIC 0.1-3.0

Includes gentamycin, vancomycin, streptomycin, kanamycin, neomycin and tobramycin. These are bactericidal and effective against many gram negative bacteria, especially those resistant to penicillins. These are potentially toxic and are administered parenterally. These drugs are used in treatment and prevention of severe infections. They act by inhibition of protein synthesis.

Mechanism of action: They combine with ribosomes and induce misreading of mRNA codons: one or more wrong aminoacids are entered in the peptide chains. When exposed to these drugs, sensitive bacteria becomes more permeable ions aminoacids and even proteins leak out, followed by cell-death.


Gentamicin (t ½ 2.0 hrs):

Administered IM as there is a better control on absorption and avoids high serum concentration. It is effective against gram positive and negative bacteria including penicillinase resistant staphylococci. The combined effects of ampicillins and gentamicin are effective against a wide spectrum of gram +ve bacteria including streptococci and staphylococci and gram-ve bacteria. Gentamicin and ampicillin should be administered separately coz gentamicin gets destroyed.

It is indicated in severe anaerobic infections.

Dose –        Adult – 3-7mg/kg/day in 2-3 divided dose.

Child – 1-3mg/kg/day in 2-3 divided dose.

Toxicity – It causes ototoxicity (vestibular and cochlear). If serum concentrations exceeds 10mg/ml transient tinnitus may occur.

When used over a weak, nephrotoxicity occurs.

Allergic reactions – not recommended in lactating mothers.

Vancomycin (t ½ 6 hours)

It has similar properties to gentamicin.

Indications – Severe orofacial infections.

Patients allergic to penicillins.

Patients with risk for endocarditis.

 

Dose:

Adult IV 500mg (IV infusion) 6th hourly or 1gm 12th hourly.

Child – 44mg/kg/day in divided doses.

Adverse reactions – Anaphyllaxis, deafness, tinnitus, hypotension and irritation at the site of injection.

Rapid administration may lead to pruritis, generalized flushing and erythrematous macular rashes and superficial thrombophlebitis.

Fluoroquinolones:

They are chemically related to nalidixic acid and have fluorine in their chemical structure and hence the name.

Commonly used fluoroquinolones are: Acrosaxacin, enoxacin, cinaxon, norfloxacin, ciprofloxacin (t ½ 3.3hrs), ofloxacin pefloxacin, lomefloxacin and sparfloxacin.

They have broad spectrum activity and bactericidal against most gram +ve and –ve organisms. Effective against staphylococci including methicillin resistant staph aureus and against streptococci including strep pneumonia. They have good activity against enterobactericae (E. coli, Klebsilla and proteus mirabilis) including many organisms which are resistant to penicillins, cephalosporins and aminoglycoside.

They are absorbed from GIT and distributed in body fluids. Most of them except pefloxacin are excreted by kidney.

These drugs except norfloxacin are useful in treating systemic and serious infections. Norfloxacin, because of low serum levels it is not effective in systemic infections, it is much effective in urinary and GIT infections.

Mechanism of action: They are bactericidal, they inhibit bacterial DNA gyrase, an enzyme which nicks double stranded DNA. The DNA gyrase reseals the nicked ends of DNA during replication or transcription.

Adverse reactions: GIT, Nausea, vomiting, diarrhea, anorexia, and abdominal discomfort CNS Toxicity – confusion nervousness, agitation and hallucinations. Allergic reactions are rare

Sulfonamides and trimethoprim:

These agents are bacteriostatic and gets inactivated by presence of pus. They act by inhibition of bacterial synthesis of folic acid from paraamino benzoic acid (PABA).

They are well absorbed by oral administration and widely distributed through all body fluids. They cross placental barriers.

They are excreted through kidneys by glomexular filtration with preferential water reabsorption. The concentration of sulfonamides in the urine is greater than in blood this leads to formation of crystals of sulfonamides termed as crystalluria and leads to renal damage. This is avoided by excessive fluid intake and by administering substances which increase urine alkalinity.

Toxic effects:

Allergic reactions – Skin rashes, exfoliative dermatitis, S-J syndrome, polyarteritis nodosa – and peripheral neuritis and photosensitivity.

Prolonged therapy can lead to macrocytic anorexia due to inhibition of conversions of folic acid to folinic acid; rarely depression of bone marrow or selective blood dyscrasias like acute hemolytic anaemia, agranulocytosis and aplastic anaemia.

Renal damage

They may also cause kernicterus by displacing bilirubin from plasma albumin in babies during intrauterine life. They may also cause foetal malformation.

These drugs present in breast milk may lead to diarrhea, rash, jaundice or kernicterus. They may also alter the actions of oral contraceptives.

Sulfadizine: It penetrates blood brains barrier. It is commonly used in traumatic meningitis.


Contrimoxazole (Sulfamethoxazole and Trimethoprim) t ½ 10-hrs

This agent inhibits the conversion of folic acid to folinic acid which is important for bacterial synthesis of DNA and RNA.

It is active against strep pyogens and most staphylococci and haemophili.

It is indicated in acute exacerbations in postirradiation osteomyelitis secondary to osteoradionecrosis. It is also used in mixed actinomycotic infections along with penicillin.

Dose 80mg of Trimethoprim + 400mg of sulfamethoxazole 2 tabs 12 hrly. Child 20mg + 100mg.

Mechanism of actions of sulfanamides:

Sulfanomides being structural analogues of PABA inhibit bacterial folate synthetase. Also being chemically similar they themselves get incorporated to form an altered folate which is metabolically injurious.


PRINCIPLES OF ANTIBIOTIC THERAPY

Principles of appropriate antibiotic use:

Several principles are to discussed that would serve as guidelines in making a decision to give an antibiotic.

  • Presence of infection: In most clinical situations, it is easy to determine if a patient has an infection. The clinical signs and symptoms of infections are pain, swelling, surface erythema, pus formation and limitation of motion. Systemically fever, lymphadenopathy, malaise, a toxic appearance and an elevated WBC counts are found, oral surgeons frequently face patients with some of the signs of infection such a situation occurs with a patient with a painful tooth but has no swelling or other signs of infection. It could be just an inflammatory condition like pulpitis, rather than an infection. In such conditions antibiotic therapy stands inappropriate.

In some patients pain and swelling observed postoperatively after a surgical removal of third molars or extensive maxillofacial surgery, the signs and symptoms of infections may not be elicited completely, it could be because of the surgery.

When a patient operated under GA develops pain and swelling along with fever but without the other signs of infection, may be because of surgical stress. Fever could be in result of insufficient postoperative pulmonary care.

Thus the diagnosis of infection and the clinicians judgement should be based on a logical process of elimination.

  • State of host defense : Host defense mechanisms are the most important factors in the final outcome of a bacterial insult. The inflammatory response and production of antibiotics provides most of this protection. If this mechanism or other host defenses are impaired, infections may result. Thus when forced with the issue of prophylactic therapy of infection, the surgeon must evaluate the general state of the host defense mechanisms.

Antibiotics help in situations in which the host has been overwhelmed by bacteria or when especially virulent bacteria are involved when defense mechanism are impaired antibiotics play a more important role in the control of infection.

The causes of depressed defenses can be divided into four categories.

Physiologic, disease related, defective immune system related and drug suppression related (anticancer drugs).

When dealing with an established infections in patients who fit into any of these categories, aggressive antibiotic therapy should be employed. Bactericidal rather than bacteriostatic antibiotics should be used.

When surgery is required in any compromised host antibiotic prophylaxis of wound infection must be considered.

  • Surgical drainage and incision:

Surgical intervention is necessary in both chronic abscess and acute indurated cellulitis. Many infections demonstrate both abscess formation and indurated cellulitis. In such situations incision and drainage of the abscess result in reduction of pressure in the area of cellulitis. It may also obviate the use of an antibiotic or may increase the effectiveness of an antibiotic as the vascular flow is restored. The host defense mechanisms are also restored with the incision and drainage.

  • The decision to use antibiotic therapy:

When the clinician is confronted with a patient with a possible infection, each of the proceeding factors must be weighed carefully. Only this can an appropriate decision be made about whether antibiotic therapy is necessary.

Minor infections in patients with depressed host defenses must be treated aggressively with antibiotics and surgery as early as possible (bactericidal) surgical intervention of the moderate or severe infections is much important along with or without use of antibiotics.

In some case like minor infections or moderate infections, where the host defense is intact surgical drainage will be sufficient without the use of antibiotics (controversial).

Principles for choosing the appropriate antibiotic:

Once the decision has made to use antibiotics as an adjunct to treating as infection, the antibiotic should be properly selected. The following guidelines are useful in making this decision.

  1. Identification of the causative organism:

The identity of a pathogen may be scientifically determined either in the laboratory, where the organism can be isolated from pus, blood or tissue or empirically based upon the knowledge of the pathogens and clinical presentation of specific infection. Antibiotic therapy is then either initial or definitive depending upon whether or not the organism is diagnosed precisely.

Initial empirical therapy can be instituted if the following criteria are met:

  • The site and feature of the infection have been well defined.
  • The circumstances leading to the infection are well known.
  • Organisms that most commonly cause such infections.

The typical odontogenic infections are caused by a mix of both aerobic and anaerobic, bacteria. About 70% of these infections are caused by this mixed flora.

Pure anaerobic infections are seen in only 25% of odontogenic infections.

Bacteria found in the well circumscribed chronic non-advancing abscess are almost always anaerobic bacteria. In cellulitis type infections aerobic bacteria is the shown cause. As the infection becomes more severe the microbiology becomes a mixed flora of aerobic and anaerobic bacteria. If the infection process subsides and controlled by the body’s defense mechanisms, the aerobic bacteria no longer survives due to hypoxic and acidotic environment.

The aerobic bacteria found in odontogenic infections are primarily gram positive cocci most of which are viridans type of streptococci. They account for approximately 85% of the aerobic bacteria found in odontogenic infections. These organisms are susceptible to penicillins and other antibiotics with an antimicrobial spectrum similar to that of penicillins.

Anaerobic bacteria, gram +ve cocci is seen in approximately 1/3rd of all odontogenic infections and other gram –ve rods are seen in 50% of odontogenic infections. The main species of the gram positive cocci are strep intermedius and peptostreptococcus species. The main gram –ve rods are porphynomonas, prevotella and fusobacterium. The fusobacterium species appear to be the most virulent and when in conjunction with strep milleri, are associated with the most aggressive odontogenic infections.

In mixed odontogenic infections

Early cellulitis is caused by streptococcus and chronic abscess is caused primarily by anerobic bacteria only. Hence the antibiotic useful for odontogenic infections must be effective against streptococcus and against anaerobes. In the later stage chronic abscess situation, anti anaerobic activity is the major antibiotic goal.

Culture should be performed in situations like compromised host defenses, patients received antibiotics for 3 days but no improvement, postoperative wound infection, recurrent infection, suspected actinomycosis and osteomyelitis. More precise information about the bacteria must be available for adequate treatment.

  1. Determination of the antibiotic sensitivity:

When treating an infection that has not responded to initial antibiotic therapy or when treating a postoperative wound infection, the causative organism must be precisely identified and the antibiotic sensitivity must be determined.

Most odontogenic infections are caused by streptococci which do not vary much in antibiotic sensitivity patterns. Staphylococcus must be treated with susceptibility information. Penicillin G can be used only if sensitivity studies supports its effectiveness, otherwise penicillanase resistant penicillins should be used. Recent reports indicate that about 20% of B.melaninogenesis is resistant to penicillins.

Penicillin is excellent for streptococcus and major anaerobes:

Erythromycin is very effective against streptococcus, peptostreptococcus and fusobacterium, clindamycin is very good for streptococcus and for the five major anaerobic groups.

Cephalexin is only moderately active against streptococcus and is good against five groups of anaerobes. Metronidazole has no activity against streptococcus but has excellent activity against the five anaerobic groups.

Several tests should be performed to provide information about the plasma level necessary to kill or inhibit growth of a bacteria by disclosing the minimal inhibitory concentration (MIC) of a specific antibiotic for the specific organisms.

  1. Use of a specific, narrow-spectrum antibiotic / selection should be based on consideration of several factors. The antibiotic with the narrowest spectrum should be choosen because if broad spectrum antibiotic is used then they might lead to resistance of other bacteria which are not involved in the infection.

The use of narrow spectrum antibiotics also minimizes the risk of superinfections.

  1. Use of the least toxic antibiotic: Select the least toxic drug from among those that are effective.

Antibiotics are used to kill living bacteria, but some antibiotics also kill or injure human cells, thus they can be highly toxic. The clinician should continuously be alert for signs of toxicity and also instruct the patient to look for and report them as well.

  1. Patients drug history:

Review of previous allergic reactions and previous toxic reactions should be done. Patients who have a history of previous major toxic or minor side effects from an antibiotic are likely to experience the same problem again. Attempts should be made to identify the drug and the precise reactions. An alternative drug should be used if possible, potential interactions with other drugs that the patient intaking must be considered. Antibiotics may prolong enhance or interface with the other medications that the patient is taking.

  1. Use of a bactericidal rather than a bacteriostatic drug:

Antibacterial therapy reduces the bacterial challenge and allows host defenses to complete the treatment.

Bactericidal is the most preferred one because of the following advantages:

  1. There is less reliance on host resistance.
  2. The antibiotic itself kills the bacteria.
  3. The drug works faster than bacteriostatic drugs.
  4. There is greater flexibility with dosage intervals.

The bacteriostatic drug exert their influence only when present in the patients tissues. Thus the bacteria resumes normal growth after the drug is eliminated.

  1. Use of antibiotic with a proven history of success:

The best evaluation of the efficacy of a drug in a particular situation is the critical observation of its clinical effectiveness over a prolonged period of time. This helps in the assessment of the frequency of treatment success and failure, the frequency of adverse reactions and the side effects. By such observations, a few drugs become standardized for use and should not be put aside for an unproven drug without good reasons.

Also, with increasing exposure, initially sensitive bacteria become more resistant to the antibiotics being used. This development of resistance to an antibiotic may be slowed by limiting its use on it may be hastened by its wide use.

Newer antibiotics should be used only when they offer clear advantages over older ones. They may be effective for bacteria against which no other antibiotic is effective, as was the case when methicilin became available for penicillinase producing staphylococcus. In such a situation, that antibiotic must be reserved for those patients with infections caused by bacteria that have a proven sensitivity to that antibiotic.

Additionally a new antibiotic may be more active at lower concentrations (thus reducing cost and dose related toxicity reactions).

  1. Cost of antibiotics: The use of a drug should always consider the patients compliance and maximum effectiveness.

PRINCIPLES OF ANTIBIOTIC ADMINISTRATION

  1. Proper dose:

The goal of any drug therapy should be to prescribe or administer sufficient amounts to achieve the desired therapeutic effect, but not enough to cause injury to the host.

The laboratory studies play an important role in helping the clinicians decision on the dose.

Determination of MIC (minimum inhibitory concentration) of an antibiotic should be done. For therapeutic concentrations the MIC of an antibiotic at the site of infection should be three to four times the MIC.

Therapeutic levels greater than 3-4 times MIC generally do not improve the therapeutic levels but rather causes likelihood to toxicity.

In situations in which the site of infection may be isolated from the blood supply as in abscess formation or in non-vital tissue, increased doses may be justified than high plasma concentrations may allow a greater amount of antibiotic to reach the sealed off bacteria by diffusion. In these cases surgical interventions must be implicated. Sufficient antibiotic must be given to reach the therapeutic levels cause the subtherapeutic levels may mask the infection and suppress the clinical manifestations without killing the bacteria and can lead to recurrence of the infection once the drug is eliminated.

  1. Proper time interval:

Just as there is a usual recommended dose of antibiotic, there is a usual recommended dosage interval, knowledge of pharmacokinetics of the drug is important.

Each antibiotic has an established half life, during which one half of the absorbed dose is excreted. The usual dosage interval for the therapeutic use of antibiotics is four times the T ½. At five times the T ½, 95% of the drug is excreted. Ex: the T ½ for cefazolin is almost 2 hours. Thus the time interval between doses should be 8 hours.

Most antibiotics are eliminated via the kidneys, the patients with pre-existing renal disease and subsequent decreased clearance may require longer intervals between doses to avoid overdosing, to maintain usual dosage schedule, excessive plasma levels and toxicity.

  1. Proper route of administration:

In some infections only parenteral administration produces the necessary serum level of antibiotic. The oral results in the most variable absorption. Most antibiotics should be taken in the fasting state to ensure maximum absorption.

In long term parenteral administration is necessary. Repeated IM is poorly accepted in patients in such situations IV is the best rate to administer.

The parenteral administration should not be changed to oral for atleast 5 to 6 days (i.e. till we get the maximum therapeutic blood levels). In mild infections it can be changed after 2-3 days.

  1. Combination antibiotic therapy:

In addition to treating infections with the most specific antibiotics possible and avoiding broad spectrum antibiotics, combination drug therapy should also be avoided. They might result in the depression of the normal host flora and increase opportunity for resistant bacteria to emerge. For routine infections, the disadvantage of combination therapy outweigh the advantages.

 

It is indicated in few situations like in:

  1. Situations of life threatening situations of unknown cause.
  2. To increase the bactericidal effect of a specific organism.
  3. Prevention of the rapid emergence of resistant bacteria.
  4. Empiric therapy of certain odontogenic infections like when the infection progresses to the lateral and retropharyngeal spaces and caused by aerobes and anaerobes.

Monitoring the patient:

Monitoring related specifically to the antibiotic therapy should be directed at the response to treatment and at the development of adverse reaction.

  1. Response to treatment:

The response to antibiotic therapy results begun by the second day and initially it is a subjective sense of feeling better. The objective signs of improvement occur with the decrease in temperature, swelling, pain and lessening of the trismus. At such time decision to be taken about the duration of antibiotic therapy. Ideally antibiotic should be given until offending bacteria is eradicated. If this is not done then there could be chance of recurrence. Careful revaluation should be done if the patient is not showing the signs of improvement special attention should be given to opt for surgical intervention. If the initial therapy fails several factors should be considered:

  1. Route of administration.
  2. Patient compliance.
  3. Correct antibiotic.

Causes of failure in treatment of infection:

  1. Inadequate surgical treatment.
  2. Depressed host defences.
  3. Presence of foreign body.
  4. Antibiotic problems – Drugs not reaching infection.

Dose not adequate

Wrong bacterial diagnosis.

Wrong antibiotic.

  1. Development of adverse reactions:

Adverse reactions occur all too commonly. Almost 15 to 20% of hospitalized patients experience adverse reactions. Hypersensitivity occurs with all antibiotics. Most common with penicillins and the cephalosporins. They manifest as accelerated anaphylactic (Type I) reactions or less severe reactions associated with edema, urticaria, itching, or they may be delayed reactions presenting only as a low grade fever. Diagnosis of anaphylaxis is not difficult but treatment must be rapid and intense.

To prevent toxicity it is important to avoid excessive dose. Therapeutic levels must be reached, but the higher the level the more likely a toxic reaction.

One toxic reaction should be discussed specifically, the problem of antibiotic associated colitis (AAC). AAC was originally associated with clindamycin therapy but has now been recognized to be caused by almost every antibiotic with the exception of the aminoglycoside. The 3 most common drugs that lead to AAL are clindamycin, ampicillin-amoxycillin and the cephalosporins. The pseudomembranous colitis is caused by toxins from clostridium difficile. Patients receiving antibiotics that alter colonic flora may have an overgrowth features of AAC. Clinical features of AAC – profuse watery diarrhea that may be bloody, crampes on abdomen, pain, fever and leukocytoss. Treatment is discontinue the antibiotics and administer anticlostridial antibiotic like vancomycin.

  1. Superinfection and recurrent infection:

The normal flora as a defense mechanism against infection, but when the flora is altered or eliminated by an antibiotic, the pathogenic bacteria resistant to the antibiotic may cause secondary infection or superinfection.

A common secondary infection in the oral cavity is candidiasis, which is primarily the result of use of penicillins. Secondary pneumonia is seen in hospital in patients who are on the broad spectrum antibiotics. Regular followup of the patient is necessary to monitor the reinfection or recurrence.

Principles of Therapeutic uses of antibiotics in maxillofacial surgery:

Maxillofacial surgeons frequently must use antibiotics in the treatment of their patients. By keeping in mind the previously discussed principles, they will be able to select those situations in which antibiotic therapy is indicated and there in which it is not.

As a general guidelines, antibiotic therapy should be reserved for those patients with clearly established manifestations of infection, that is fever, malaise, swelling and pain. Such patient should be treated surgically as early as possible.

Abscess – Surgical interventions and antibiotics.

Pericoronitis – Preoperative antibiotics and surgery and postoperative antibiotics.

Osteomyelitis – Preoperative antibiotics and surgery nd postoperative antibiotics.

Fractures – Immediate preoperative antibiotics and surgery and postoperative antibiotics.

Soft tissue wounds – Debridement and toileting later antibiotics.

Principles of Prophylactic antibiotics:

The use of antibiotics for prevention of infection is clearly established and it not accepted widely.

Infection prophylaxis obviously has many advantages:

  1. Prevention of infection.
  2. Decrease patient morbidity and mortality.
  3. Decrease hospital stay.
  4. Decreased medical cost.
  5. Decreased total antibiotic usage.
  6. Decrease numbers of resistant bacteria – because of short term course.

Disadvantages:

  1. No reduction of infection.
  2. Development of increased number of resistant bacteria.
  3. Delay in onset of infection.
  4. Adverse effect on surgical technique.

The most effective method which can be practiced is a “short term administrations of a narrow spectrum antibiotics”.

In order for prophylaxis antibiotics to be effective a set of well established guidelines must be followed. The principles for prophyllactive antibiotics are:

  1. The operative procedure must have a risk of significant bacteria contamination and a high incidence of infection.
  2. The organism most likely to cause the infection must be known.
  3. The antibiotic susceptibility of the causative organism must be known.
  4. To be effective and to minimize adverse effects the antibiotic must be in the tissue at the time of contamination (operation) and it must be continued for not more than 4 hours after cessation of contamination.
  5. The drug must be given in dosages sufficient to reach four times the MIC of the causative organisms.
  6. Time the antibiotic correctly.
  7. Use the shortest effective antibiotic exposure.
Posted in General Medicine for OMFS

Suture Materials

SUTURE MATERIALS USED IN ORAL & MAXILLOFACIAL SURGERY AND PRINCIPLES OF SUTURING

INTRODUCTION

Closure of the wound is one of the most important aspect of any operation and yet it is frequently one that is given least attention.

It is said that most common cause of postoperative infections is poor surgical techniques, usually related to devitalized tissues remaining in the wound and also inadequate closure.

Thus closure of wound by suturing helps to obliterate dead space where accumulation of blood or other tissue fluids could prevent direct apposition of tissues and provide an environment favourable for bacterial growth. Sutures also distribute the tension of wound closure over a larger volume of tissues.

Sutures have been used to close wounds as early as 50,000 B.C. It is said that an old method of wound closure has been using large black ants, which bite the wound edges together and the ants body being twisted off leaving the head in place.

A sutures is any thread or strand which brings into apposition no surfaces or tissues, while a ligature is any thread or strands obliterates the lumen of ductular structures. Characteristics of this elusive material are non-reactivity, retention of tensile strength until healing has occurred and easy handling.


CLASSIFICATION OF SUTURE MATERIALS

  • Absorbable:
  1. Natural
  2. Catgut           Pain

Chromic

  1. Fascia Lata
  • Kangaroo tendon
  1. Beef tendon
  2. Synthetic
  3. Polyglactin 910
  4. Polyglycolic acid
  1. Polyglecaprone 25 (monocryl)
  • Non-Absorbable:
  1. Natural silk, cotton, linen.
  2. Polyamide
  3. Monofilament
  4. Polyfilament (braided)
  5. Polyester – Polyfilament
  6. Coated (with polybutylate)
  • Polypropylene – monofilament (prolene)
  1. Polybutester – novafil.

 

  1. Metals:
  2. Stainless steel.
  1. Silver wire.

ABSORBABLE SUTURES:

Gut / Catgut

Gut is the oldest known absorbable suture material. It is a misnomer and has been derived from sheep intestinal submucosa or bovine intestinal serosa.

The origin of the word catgut is Arabic ‘KITSTRING’ or ‘KITGUT’, it is prepared from the submucosa of the sheep’s intestine. Submucosa of sheep has a rich elastic tissue content which accounts for high tensile strength of the catgut. It is monofilament and is available in the plain form as well as “tanned” in chromic acid. The tanning process delays the digestion by white blood cell lysozymes.

Sterilization:

Catgut should not be boiled or autoclaved as heat destroys the tensile strength. Catgut is sterilized during preparation and kept in a preservative solution (ethicon fluid contains 2.5% v/v formaldehyde plus 87.5% v/v denatured absolute alcohol) inside spools or foils. Unused and reusable catgut is hygroscopic so, catgut will swell due to water absorption and its tensile strength will be reduced (previously iodine method and chromic acid method were use for sterilization).

It is available pre-sterilized in aluminium-coated sterile foil overwrap pack with ethicon fluid as a preservative.

Colour: Plain catgut is yellow, while chromic catgut is tan.

Duration of gut in body tissues: Plain catgut retains its tensile strength for approximately 10 days, while chromic catgut for 20 days. Tensile strength of chromic catgut is zero after 30 days and gets absorbed completely in 100 days.

Absorbtion: Catgut is absorbed by proteolytic digestive enzymes released from inflammatory cells collected around the catgut. So, in the presence of infected catgut is rapidly absorbed.

Size: Catguts are made of varying thickness and according to the thickness, they are numbered like 1-0, 2-0 etc. as per BPC gauge system. The bigger the number the lesser. The thickness and smaller the number more the thickness.

Uses: Plain catgut is used for ligation of smooth blood vessels near skin surface and to suture subcutaneous tissue.

Chromic catgut:

1-0/2-0 : Used for ligation of medium sized blood.

3-0/4-0 : To close muscle layer in cleft lip repair.

5-0/6-0 : In plastic surgery.

AVAILABILITY

  • Plain Catgut:
  1. On needle – The curved needle may be round or cutting the curves of the needle body are ½, 3/8 and 5/8 of circles. Sizes are 6-0 to 2-0, length is 76cms, except No. 6-0 which is 38 cms long.
  2. Without needle: Size 5-0 to 4-0, length is 152cms strands are available in pieces e.g. Two pieces / three pieces.
    • Chromic catgut:
  3. On needle – Size 6-0 to 2-0, length is 76 cms except No. 6-0 which is 38 cms long. Needle may be curved or straight. Curved needles may be round bodied / cutting. Single armed / double armed and circle may be ½, 3/8 or 5/8.
  4. Without needle: Length is 152cms, size is 5-0 to 4-0 strands are available as one piece, two piece or three pieces.

POLYGLYCOLIC ACID (DEXON) :

It is a synthetic and absorbable suture material. It is a non-protein polymer of glycolic acid.

Absorption: By esterase enzyme system.

Packing: Available in pre-sterilized form in foil overwrap without a preservative.

Characteristics: It is white in colour and polyfilament braided suture.

Length: 76cms, available on needle.

Absorption time: 100 days.

Tensile strength is maintained for 30 days.

Advantages:

  • Minimum tissue reaction.
  • Less tissue oedema.
  • Uniform absorption.
  • Can be used in the presence of infection.
  • Better knot holding properties (braided).
  • Less fraying of ends (braided).

POLYCLACTIN 910 (Vicryl):

It is a synthetic absorbable suture material. Polyglactin 910 is a co-polymer of glycoline and lactide. It is braided to improve handling and is coated to reduce bacterial adherence and tissue drag.

Colour : Violet.

Size: 7-0 to 1-0.

Length: 7-0-30cms, 6-0 to 3-0 – 45cms, 2-0 to 1-0, 90cms.

Advantages: Minimum tissue reaction (It is synthetic)

  • No fraying.
  • Excellent handling characteristics.
  • Its distinct violet colour is highly visible in the wound.
  • Its unique molecular structure causes it to retain its strength over the critical healing period and then to be absorbed rapidly after suture has served its function.
  • Can be used in presence of infection.

Disadvantages: Only disadvantages is its roughness (causes swelling action).

Absorption: It is disintegrated by hydrolyses and then pieces of filaments are phagocytosed by PMN and other macrophages. Due to this, there is least tissue reaction and absorption is not affected by presence of infection.

Absorption is minimal until the 40th day. It is essentially complete between 60th and 90th days.

Tensile strength : Approximately 55% of original tensile strength of vicryl remains at 14 days and 20% at 21 days.

VICRYL RAPIDE (Irradiated Polyclactin 910)

It is braided synthetic absorbable suture material.

Colour: White.

Wound strength : It has a similar initial high tensile strength as that of the normal vicryl suture. It gives wound support upto 12 days. It shows 50% of the original tensile strength after 5 days and all of its tensile strength is lost after 14 days. Its absorption is associated with minimal tissue reaction facilitating improved cosmetis and reduction of postoperative pain. The absorption is essentially complete within 35-42 days.

Uses: Ideal for intra-oral use.

POLYGLECAPRONE 25 (MONOCRYL)

It is a monofilament, synthetic, absorbable suture.

Composition. It is a co-polymer of 75% glycolide and 25% caprolactone.

Colour: Golden.

Wound strength: It has a high initial tensile strength, which is double that of chromic catgut when placed in tissue. After 7 days post implantation approximately 50-60% of the original tensile strength remains. At the 14th postimplantation day, approximately 20-30% of the original strength remains, with wound support continuing upto 21 days.

Absorption: It is broken down by hydrolysis. The time required for absorption to be complete and 90-120 days postimplantation.

Advantages: High tensile strength.

  • More predictable wound strength and absorption characteristics.
  • Absorption is by hydrolysis, so it is not affect by infection.
  • Relatively inert.
  • Smooth surface so glides through the tissue with minimal effort.
  • Monofilament sutures reduces the chance of infection.
  • It is virtually memory free, so it can be controlled by a surgeon when suturing or ligating.

Disadvantages: Cost.

Indications:          Subcutaneous closure

Subcuticular closure

Available sizes: 5-0 to 1-0.

POLYDIOXANONE SUTURE (PDS):

It is a synthetic, absorbable suture material. Total absorption takes 240 days. Mechanism of absorption is same as that of vicryl.

Tensile strength: 70% tensile strength remains at 20 days, at 40 days and 20% at 60 days.

COTTON THREAD: It is a natural, non-absorbable suture material of vegetable origin. It is a twisted polyfilament available in reels in an unsterile form.

Sterilization: long pieces of thread are wound around a rubber tube and autoclaved.

Sizes: 2, 8, 10, 20, 40, 60 and 80: No. 2 is the thickest and 80 the thinnest.

Advantages: Cheapest and freely available; Secure knotting and easily handled.

Disadvantages: Absorbs fluids by capillary action, so more chances of infection.

  • Tissue reaction is more.
  • Frays easily and has low tensile strength.

LINEN: It is a natural, non-absorbable, polyfilament suture material of vegetable origin made from jute fibres. Though costlier, it is preferable to cotton.

Colour: Natural linen colour. Pack is pink colour.

Size: Thickest No. 20; thinnest No. 80.

Advantages: It is easily handled : Knots slide down smoothly and tie securely.

SILK: Natural, non-adsorbable, polyfilament suture material, obtained from the cocoon of silkworm. It loses its tensile strength in about a year and is completely removed from the operative site in two years. So, its actually an absorbable material.

Size: No. 2 thickest, and No. 80 thinnest.

Advantages:

  • It does not soak up fluids and never becomes limp or brittle.
  • It ties down smoothly and securely and its natural elasticity gives it an extensibility that signals when optimum knot replacement has been achieved.

Disadvantages : Stitch granuloma.

Infection rate is high as compared to synthetic materials.

Availability : In sterile foil overwrap pack as eyeless needled sutures. As sutupac-precut lengths of sterile sutures, in a pack of 2 & 6 pieces of suture material, without needle. On reels – nonsterile.

Colour : Black.

Types: According to preparation.

  • Perma hand surgical silk.
  • Virgin silk suture which is prepared from the glands of silk worm before their pupae stage.

According to fibre pattern:

Uses: To ligate blood vessels and pedicles.

  • To suture nerve.
  • To suture grafts in vascular surgery (atraumatic silk).
  • To suture tendons.
  • Skin suture.
  • For fixing skin grafts.
  • Suturing of wound over face.

NYLON: It is a synthetic, non-absorbable suture. It may swell up in tissues and lose some of its tensile strength after a year. Its thickness varies from 1N to 8N.

Advantages:

  • Less irritant.
  • High tensile strength, which is retained for a long period. Its tensile strength is expressed in terms of weight in pounds it can suspend. E.g., 1 pound, 6 pounds etc.

Disadvantages:

  • Knot is slippery, so 5-7 knots should be applied.
  • Infection due to crevices in braided nylon.
  • Too smooth and stiff knots likely to slip.

PROLENE: It is made up of a polymer of propylene. It is a synthetic, non-absorbable suture.

Advantages:

  • It is as inert as steel and resists breaks by infection.
  • Monofilament, so less chances of infection.
  • High degree of smoothness, so it requires much less force to draw through the tissue.
  • Its sky blue colour has high visibility in tissues.
  • It is pliable, so it ties securely and can be easily handled.
  • Knot security – plastic deformity enables the knot to flatten out and lock against itself.
  • Least thrombogenic, so an important factor in vascular surgery.
  • It will retain its tensile strength for years.
  • It is unwetted by blood, unweakened by tissue enzymes and offers prolonged tensile strength, even in infected areas.
  • More elastic.

Availability : In pre-sterilized foil overwrap pack as eyeless needled sutures.

Size: 7-0 to 10-0.

Length : 70 cms.

Uses: Plastic surgery.

Vascular surgery for anastomosis between vessels.

Sterilization: Available pre-sterilized; sterilized in ethicon fluid when it is to be re-used.

Stainless steel wire: It is made up of stainless steel. It excites very little tissue reaction.

Disadvantages: Cutaneous discomfort, knots are not firm and may break.

Sizes : 25 to 40 wire gauge.

Sterilization : Autoclaving.

POLYAMIDE (ETHICON)

It is a synthetic, non-absorbable suture. It is monofilament polyamide.

Colour: black.

Advantages:

  • Minimal tissue reaction.
  • Remarkably smooth, so preferred for subcuticular stiches.
  • High degree of elasticity with secure knot tying extremely strong.

Size 10-0 to 1-0.

Length:       10-0 to 8-0 ; 25 cms and 38 cms.

6-0 to 1-0 ; 70 cms.

It is available in sterile foil packing as eyeless needled sutures.

10-0 to 8-0 are used in microsurgery

6-0 to 3-0 are used in plastic surgery.

Polyamide is also available as braided polyfilament.

SUTUPACK: It is available as two or more pieces of suture material without a needle. Two types are available – silk and nylon.


Expanded PTFE (Gortex):

It is a non-absorbable, monofilament suture. Expands causes a porous micro-strucutre which is more than 50% air by volume.

Advantages:

  • Inert – minimal tissue reaction.
  • Does not degrade in the presence of infection.
  • Fibroblasts and leukocytes infiltrate into internodal spaces, thus re-inforcing the strength.

NEWER NON-ABSORBABLE SYNTHETIC SUTURE MATERIAL

Dacron

PTFE (Gortex)

Mersidene (Orange)

Maxon

Marlex

Ethibond

Polyglyconate (green)

Polyethylene

Polyester

PRINCIPLES OF SUTURE SELECTION

The selection of a suture material by a surgeon must be based on a sound knowledge of the healing characteristics of the tissues which are to be approximated, the physical and biological properties of the suture materials, the condition of the wound to be closed and the probable post-operative course of the patient.

  • When a wound has reached maximal strength, sutures are no longer needed. Tissues that heal slowly such as skin, fascia and tendons should usually be closed with non-absorbable sutures. Tissues that heal rapidly such as peritoneum, liver, small intestines, muscles, stomach, colon and baldder may be closed with absorbable sutures.
  • Multifilament sutures should be avoided in contaminated wounds as bacteria can linger within them and may convert it into an infected one.
  • Where cosmetic results are important, close and prolonged apposition of wounds and avoidance of irritants will produce the best results. So, the smallest inert monofilament suture materials such as polyamide or prolene should be used. Skin sutures should be avoided and subcuticular closure should be performed wherever possible.
  • Intra-orally, multifilament braided materials such as black silk, or absorbable synthetic materials such as polyglycolic acid and polyclactin, are flexible and preferable for use. Of these, absorbable sutures are more preferable as they spare the patient the discomfort of having the sutures removed and an inconvenience of an additional visit to the clinic and are especially important when dealing with children. The optimum time for spontaneous suture loss intra-orally is 5-14 days and an ideal materials which satisfies this criteria more or less is vicryl rapide.


NEEDLES:

Proper suturing begins with an understanding of the physical and biologic properties of both the needle and suture material.

The surgical needles are sharp, pointed instruments used for puncturing the tissue for guiding the thread or wire to suture or pass a ligature around the vessels. They are available in a wide range of types, shapes, lengths and thickness.

Needles are either made of stainless steel or carbon steel.

 

ANATOMY OF SURGICAL NEEDLES:

Classification of Surgical Needles:

  1. According to its eye:
  1. Eyeless needles.
  2. Needles with eye.
    1. According to shape:
  3. Straight needles.
  4. Curved needles.
    1. According to cutting edge:
  5. Round body needles.
  6. Cutting needles
    1. Conventional cutting needles.
    2. Reverse cutting needles.

 

  1. According to its tip.
  1. Triangular tipped needles.
  2. Round tipped needles.
  • Blunt point needles.
    1. Others:
  • Spatula needles.
  • Micropoint needles.

EYELESS NEEDLES:

One strand of suture material is attached to the swage of a needle during manufacturing.

It has the following advantages.

  1. Causes minimal tissue trauma as only a single swaged suture strand is drawn through the tissue.
  2. Each patient has the benefit of a new sharp needle. Reusable needles are potentially dull, blurred or tarnished.
  3. these needles do not unthread and can be easily recovered it accidentally dropped.
  4. Allows faster, more efficient surgery.

NEEDLES WITH EYE

The only advantage is that as it can be re-used, it is cheaper.

Straight needles: Available both as eyeless and with eye and round body and blunt tip.

  • Particularly used to suture skin and fascia.
  • Intra-orally (Oral & Maxillofacial surgery), used for the passage of circum-zygomatic and circummandibular wires.

 

 

 

CURVED NEEDLES: Available as eyeless and with eye and round body and cutting needle.

Needles traverses the tissue with circular movement and facilitates working in depth.

The more confined the operative site the greater the curvature required.

Manufactured with varying curvatures – 1/8, ¼, ½, 3/8 and 5/8.

ROUND BODY NEEDLES:

They are designed to separate tissue fibres rather than cut them and are used for soft tissues like muscle and fascia, or in situations where easy splitting of tissue fibres is possible. After the passage of needle, the tissue closes tightly and the suture material, thereby forming a leak proof suture line, which is particularly vital in intestinal and cardiovascular surgery.

MAYO’S NEEDLE: It is a strong round body needle with a round tip used to penetrate periosteum.

CONVENTIONAL CUTTING NEEDLE: The point of this needle is triangular in cross-section with the apex cutting edge on the inside of the needle curvature. It is used for keratinized mucosa, skin or subcuticular layers where the tissue is difficult to penetrate.

REVERSE CUTTING NEEDLE: The body of this needle is triangular in cross-section with the apex cutting edge on the outside of the needle curvature. This improves the strength of the needle and particularly increases resistance to bending.

TROCAR POINT NEEDLE: This needle has a strong cutting head, which merges into a robust round body. The design of the cutting head is such that it ensures powerful penetration even when deep in the dense tissue.


PRINCIPLES OF SUTURING

  1. The needle holder should grasp the needle at approximately 1/4 of the distance from the point.
  2. The needle should enter the tissue perpendicular to the surface. If the needle pierces the tissue obliquely, a tear may develop.
  3. The needle should be passed through the tissue following the curve of the needle.
  4. The suture should be placed at an equal distance from the incision on both the sides and at an equal depth. This principle can be modified in cases where the tissue edges are at different levels; then passage of the suture closer to the edge of the lower and farther from the edge of the higher side will tend to approximate the levels. Another method involves passage of the suture at an equal distance form the wound margins on both sides, but deeper into the tissues on the lower side and more superficially on the higher side.
  5. The needle should pass from the free tissue to the fixed side.
  6. If one tissue side is thinner than the other the needle should pass from the thinner tissue to the thicker one.
  7. If one tissue plane is deeper than the other, then the needle should pass from the deeper to the superficial side.
  8. The distance that the needle is passed into the tissue should be greater than the distance from the tissue edge.
  9. The tissues should not be closed under tension, since they will tear or necrose around the suture. If tension is present the tissues should be undermined to relieve it.
  10. The suture should be tied so that the tissue is merely approximated and the edges are everted.
  11. The knot should not be placed over the incision line.
  12. Sutures should be placed approximately 3-4mm apart. Closer spaced sutures are indicated in areas of tension.
  13. If “dog ear” occurs at the end of incisions, it should be eliminated.

“Dog ear” elimination:

Excess tissue is undermined and an incision is made at approximately 30 degrees to the parent incision directed towards the undermined side. The extra tissue is pulled over the incision and the appropriate amount is excised. Closure is then achieved in normal manner Another method includes excising the excess tissue with an elliptical incision and then achieving closure in the normal manner.

KNOT TYING:

The surgeon may use either the instrument tie or one or two hand tie. The instrument tie is more convenient in closed areas such as mouth, but can be used in open areas as well. Therefore adequate knowledge of this technique is recommended.

SQUARE KNOT: The basic knot is the square knot and requires at least three ties for surface knots. It is formed by wrapping ties around the needle holder once in opposite directions between ties.

SURGEON’S KNOT: Because of the double throw, the surgeon’s knot offers the advantage of reducing slippage of the first tie, while the second tie is put in place. This is particularly useful in confined or difficult to reach places where the first tie would ordinarily be loosened in the process of producing the second tie. A third tie squared on the surgeon’s knot is usually made for security. This method is modified for use with polyglycolic acid and synthetic sutures.

GRANNY KNOT: This knot involves a tie in one direction followed by a single tie in the same direction as the first. A third tie is then squared on the second to hold the knot permanently.

SUTURE METHODS

Some of the commonly used suturing types:

  1. Interrupted methods.
  2. Continuous suture.
  3. Locking continuous suture.
  4. Mattress suture.
  5. Figure of 8 suture.
  6. Subcuticular suture.
  7. Tension suture.
  1. Interrupted suture:

The interrupted suture is the most commonly used and it is preferred in areas of tension over continuous sutures.

Advantages:

  1. It is strong and successive sutures can be placed in a manner to fit the indirect requirements of the situation.
  2. Each suture is independent of the next and loosening of one suture will not cause loosening the others.
  • A degree of eversion of the incision can be produced by ensuring that the depth of the bite is greater than the distance from the suture of the wound edge, should the wound become infected, removal of a few selected suture may be satisfactory treatment..


  1. CONTINUOUS SUTURE:
    • The continuous suture provides a rapid technique for closure.
    • Provides even distribution of tension over the entire suture line.
    • Provides a more watertight closure, which is especially important in intra-oral bone grafting.
    • It should not be used in areas of existing tension.

Method: A simple interrupted suture is placed and needle is then inserted in continuous fashion. The suture passes perpendicular to incision line underneath tissue and diagonally on surface and is ended by tying to last untightened loop of suture.

LOCKING CONTINUOUS SUTURE

This technique offers two advantages over the simple continuous technique:

  1. The suture will align itself perpendicularly to the incision.
  2. The locking feature prevents continuous tightening of the suture as wound closure progresses.

Here, care should be exercised not to tighten the individual lock excessively, since this can produce tissue necrosis.

Also, the locking feature may prevent adjustment of tension over the suture line as tissue swelling occurs.

Method: Suture is passed perpendicular to incisor line and degree of locking is provided by withdrawing suture through its own loop. The suture technique is begun and ended identically to continuous technique.


MATTRESS SUTURE :

Mattress sutures are of two types –

Vertical & Horizontal.

Techniques:

Vertical : needle is passed close to incision line on both sides and then engages tissue deep to first pass when returning towards the original side.

Horizontal: Suture passes perpendicular to incision line underneath tissue and parallel to it on the surface and then again perpendicular to incision line underneath tissue to be knotted on that side.

A mattress suture is used to provide more tissue eversion and is used in areas when wound contraction could cause dehiscence and broad soar formation. The vertical mattress suture offers the advantage of running parallel to the blood supply of the edge of the flap and therefore not interfering with healing.

The interrupted horizontal mattress suture produces broad contact of the wound margins and is useful where such a condition is needed. However, it suffers from the disadvantage of constricting the blood supply to the edges of the incision.

A continuous horizontal mattress suture is often used after intra-oral bone grafting, as the eversion and continuity provide a very watertight closure.


FIGURE OF EIGHT: The figure of 8 suture is used over extraction sites where it provides some protection to the socket as well as adaptation of the gingival papillae round the adjacent teeth.

SUBCUTICULAR SUTURE:

  • An absorbable 4-0 suture material is generally used for closure of the subcuticular layer.
  • If individual subcuticular sutures are placed, they should be buried with the knot inverted.
  • A continuous subcuticular suture can be used with no knots by having the ends exist a short distance from the wound and taping to the skin.
  • In this technique non-absorbable sutures are usually used.
  • Free passage of the suture along the incision to facilitate subsequent removal is ensured by pulling the ends after placement.
  • A continuous subcuticular suture may be left for 7-10 days and removed by pulling in one direction.

TENSION SUTURE: This type of suture is used to prevent wound dehiscence. A suture materials of good strength like non-absorbable nylon or prolene is used with a plastic tubing to reduce the tension exerted by the sutures on the tissues.

SUTURE REMOVAL: When sutures are removed, suture should be grasped with an instrument elevated above the epithelial surface.

A scissors should be used to transect side of the loop as close to the epithelial surface as possible. In this way a minimal amount of the portion of the suture that was exposed to the outside environment and has become laden  with debris and bacteria will be dragged through the tissue.

OTHER SUPPLEMENTS / ADJUNCTS TO WOUND CLOSURE

  1. Skin staples: Skin staples are particularly used for long incisions as a time saver or to position a skin closure or flap temporarily before suturing. Grasping the wound edges delicately with forceps to evert the tissue is helpful when placing the staple to prevent inverted skin edges.

Staples must be removed early to prevent inverted skin marks and are therefore best used in hair bearing scalp.

  1. Skin tapes : Skin tapes can effectively approximate the wound edges, although buried sutures are often required in addition, to approximate deeper layers, relive tension, and prevent inversion of the wound edges. As skin sutures are ideally removed within 5 days. If adequate intradermal suturing has been performed, this guideline can be followed in any area of the body.
  2. Tissue adhesives.

Cyanoacrylates, the tissue adhesive component of many commercially available glues has been used by the medical profession for various purposes, including tissue adhesion, embolization, hemostasis, osteosynthesis and as wound dressing material.

Cyanoacrylates are quick-setting, biodegradable, polymeric tissue adhesives that have become useful tissue bonding agents.

They form a strong, durable bond with most human tissues, particularly those that contain a large amount of protein such as skin and tendon.

The cyanoacrylates tissue adhesives polymerize by an exothermic reaction in the presence of water and hydroxyl groups on the wound surface and thus are effective on moist surfaces.


ADVANTAGES OF CYANOACRYLATE TISSUE ADHESIVE INCLUDE:

  1. Effective and immediate hemostasis.
  2. Bacteriostatic properties.
  3. Rapid adhesion of hard and soft tissues.
  4. Significantly less pain and oedema.
  5. Better aesthetics when compared to sutures.

Disadvantages:

  1. Low tensile strength.
  2. After polymerization, the tissue adhesive is brittle and can fragment if flexed over a joint crease.

TISSUE REACTION TO SUTURES:

The initial body response to sutures is almost identical in the first 4 to 7 days, regardless of the suture material. The damage done to the tissue by the needle evokes a significant inflammatory response even without the presence of suture material. After 4 to 7 days the response is more related to the type of suture material.

If the suture material leads to mucosal or skin surfaces, epithelial cells will begin tracking down the suture pathway at 5 to 7 days. The longer the suture remains the deeper the epithelial invasion of the underlying tissue. When such sutures are removed an epithelial tract remains. These cells may eventually disappear or remain to form keratin and epithelial inclusion cysts. The epithelial pathway may also cause the site of the sutures to be visible and the typical “railroad track” scar results.

The development of surgical infections is greatly enhanced by the presence of a suture in a contaminated wound. The use of monofilament sutures rather than braided sutures reduces the potential for infection as the multifilament sutures provide a haven for bacteria, which can penetrate the interstices of the suture that are too small to allow granulocytes and macrophages. As a general rule, sutures should not be used in the presence of infections and should be removed if an infection becomes evident.

All sutures passing through the mucous membrane or skin provide a “wick” down through which bacteria can gain access to the underlying tissues and may cause inflammation possibly leading to granuloma formation or a stitch abscess. Because of this and the downward growth of the epithelial tissue, the sutures should be removed as early as possible consistent with adequate healing. Generally, sutures should be removed after 3 to 5 days on the skin of the head and neck, 5 to 7 days intra-orally, 5 to 10 days in other sites, and longer for areas subjected to considerable stress, such as over joints or the iliac crest, or in areas of slower healing such as the palms or soles. In cancer patients, the sutures should be removed on the 14th day.

At the 5th to the 7th day when sutures are most often removed, there is relatively little tensile strength of the wound and that which is present is due to adhesiveness of cells, blood vessels, globular proteins, and fibrin not to formation of collagen. At least 5 to 42 days are required for significant collagen synthesis to occur. Therefore, cutaneous wounds should be supported with sterile tape following suture removal.


SUMMARY & CONCLUSION

Choice of appropriate suture for a given wound should be based upon principles of wound care. In wound closure, the surgical technique is far more important than the sutures used but a good scientific knowledge of different sutures and needles and how they perform, will aid the surgeon to achieve optimum wound healing. Since suture technology has kept pace with advances in surgical techniques, it is imperative on the part of the surgeon not only to be fully aware of them but also to keep them in their surgical armamentarium.


REFERENCES

  1. Oral & Maxillofacial Surgery. Vol. I : By Daniel M. Laskin.
  2. General Surgical Operations: By R.M. Kirk.
  3. Grabb & Smiths : Plastic Surgery.
  4. Plastic Surgery : Mc Carthy.
  5. Textbook of Surgery : Sabiston.
Posted in General Medicine for OMFS

Pain Physiology

 

Introduction

Pain is probably the most fundamental and primitive sensation. It is distributed more or less all over the body. It is protective in nature and always indicates some serious trouble in the locality, such as a structural damage or a serious functional or metabolic derangement.

 

Definition

It is difficult to define pain, as the feeling is purely subjective. It may be succinctly described as ‘what the patient says it hurts’. Dorland’s Medical Dictionary (1974) defined pain as ‘more or less localised sensation of discomfort, distress or agony resulting from the stimulation of specialised nerve endings’. Fields (1987) defined pain as ‘an unpleasant sensation that is perceived as arising from a specific region of the body and is commonly produced by processes which damage or are capable of damaging bodily tissue’. In other words, pain is a somatopsychic phenomenon.

The definition proposed by the Subcommittee on Taxonomy (1986) of the International Association for the Study of Pain (IASP) is that ‘pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage’. Added to this definition is a note to emphasise the subjective nature of pain that distinguishes and separates it from a simple stimulation of nociceptors.

 

Types of pain

Many researchers have tried to classify different types of pain, and have observed various varieties.

Clinical vs. Experimental pain

Beecher (1956) has pointed out that pain as presented by patients, so-called clinical or pathological pain is different from experimental pain induced and studied in the laboratory. The difference is illustrated in the capacity of morphine to give relief. Large doses of morphine does not significantly alter the brief jabs of experimental pain, whereas a much smaller dose consistently reduces pain that has a meaning to the patient.

Acute vs. Chronic pain

As the duration of pain input continues, the level of suffering increases even though the intensity of input remains the same. In fact, a protracted input may sustain a high level of input although the intensity of stimulus decreases or disappears altogether. Pain becomes complicated and difficult to manage when it is prolonged. In chronic pain, it is common to see a wide discrepancy between the identifiable nociceptor source, and the amount of suffering and disability.

Somatic pain vs. Neurogenic pain

Pain emanating from a particular area may result from noxious stimulation of the somatic structure, the nociceptive receptors, being received and transmitted by normal components of the sensory nervous system. Such pain is referred to as ‘somatic pain’. Quite a different type of pain may emanate from the same area not due to abnormality in the structures that comprise that area, but due to the abnormality in the neural component that innervate the area. Such pain is known as ‘neurogenous pain’.

Superficial pain vs. Deep somatic pain

Pain emanating from the cutaneous or mucosal tissues present clinical characteristics that are similar to the other exteroceptive sensations. They are precisely localisable and relate faithfully to provocation in timing, location and intensity. In contrast, pain due to stimulation of deeper somatic and visceral structures resemble other proprioceptive and interoceptive sensations. They are more diffusely felt and are less responsive to provocation, and frequently initiate secondary effects such as referred pain and muscle spasm activity.

Primary and secondary pain

If the pain emanates from the structures that hurt, it constitutes a primary nociceptive input. If the true source of pain is located elsewhere, and the heterotropic referred pain (secondary hyperalgesia) is felt in otherwise normal structures, the area of discomfort represents secondary pain.

Musculoskeletal vs. Visceral pain

Pain that emanates from muscles, bones, joints, tendons, ligaments and soft connective tissue bears a close relationship to the demands of biomechanical function. Such pain also yields a graduated response to noxious stimulation. Visceral structures, however, are innervated by high threshold receptors so that pain is usually not felt until threshold level is reached. Such pains therefore do not ordinarily yield a graduated response to noxious stimulation and are not responsive to biomechanical function.

Inflammatory pain vs. Non-inflammatory pain

Tissue injury and healing are attended by an inflammatory reaction that includes pain. Such pain relates to the location, type and phase of inflammatory process that prevails. Inflammatory pains therefore display a clinical timeframe that relates to the inflammatory curve, and symptoms that relate to the confinement of inflammatory exudate. Non-inflammatory pains do not display this type of behaviour.

Spontaneous pain vs. Stimulus evoked pain

Most primary somatic pains result from stimulation of neural structures that innervate the site. Some pains occur spontaneously and do not require a stimulating force. Neurogenous pain may be felt spontaneously along the peripheral distribution of the affected nerve, while referred pains may occur spontaneously as far as the site of pain is concerned.

Sensory reception

Pain is essentially an abnormal affective state that is aroused by the pathological activity of a specific sensory system. Though it has proved difficult to investigate, it is known that it is subserved by its own network of nerve fibres. Morphological structures of the end organs subserving pain sensations are not clear. Naked nerve endings are presumably the sense organs of pain, and are distributed all over the body.

There are evidences suggesting that the pain receptors are modality-specific. Pain is not produced by overstimulation of other receptors. Possibly there are specific receptors for subserving pain sensation by specific pain stimulus, i.e. some respond to thermal, others to mechanical and still others to chemical stimulation.

Physical stimulus

Pain is produced in the skin by many kinds of physical stimuli – thermal, mechanical or electrical – which have the common property of being potentially or actually harmful. The pain accompanying protective reflexes and voluntary responses minimise the amount of damage inflicted by the noxious stimulus e.g. raising skin temperature to 45˚C or more, exposure to cold at 0˚C, excessive pressure or tension on the surface of the body etc.

Transmission of impulses

Pain sensations are transmitted by two types of fibres – slow fibres and fast fibres. The slow fibres are unmyelinated dorsal root C (d.r.C) fibres having a slow rate of conduction (0.5 – 2 m/sec) and a diameter of 0.4 to 1.2 mm. The fast fibres are the small myelinated A-d fibres having a diameter of 2–5 mm, and a conduction velocity of 12 – 30 m/sec. According to the presence of separate types of pain fibres and also of different conduction velocity, pain ahs been classified into two – slow and fast.

The cell bodies of both fibre groups lie in the dorsal root ganglia of the spinal cord; A-d fibres terminate primarily on neurons in laminas I and V, whereas the dorsal root C-fibres terminate on neurons in laminas I and II. In the case of cranial nerves, the fibres end in their respective sensory ganglia.

Neurochemical effects

The biochemical basis of nociception is becoming better understood. The presence of a specific chemosensory pain mechanism in the human skin was described by Dash et al (1971). Several chemicals play important role in the neural mechanism of pain. Some of these act principally as algogenic (pain producing) agents, some act centrally as neurotransmitters and some act in both capacities.

1.   Prostaglandins

These are a group of organic acids chemically related to long-chain hydroxy-fatty acids. There are six types, each designated by a suffix letter. Subscript numerals indicate the degree of saturation of the side chain. Prostaglandin E2 occurs in conjugation with inflammatory process. They sensitise the nociceptor nerve endings to different types of stimuli, thus lowering their pain threshold to all kinds of stimulations. Prostaglandins are required for bradykinin to act. Bradykinin, in turn, stimulates the release of prostaglandins. There is evidence that prostaglandin-like substances are produced in the CNS during an inflammatory reaction that produces hyperalgesia.

2.    Bradykinin

This is an endogenous polypeptide released as a part of an inflammatory reaction. It is a powerful vasodilator and increases capillary permeability. It sensitises some high threshold receptors so that they respond to innocuous stimuli, such as that occurs during normal activities. It requires the presence of prostaglandins to act.

 

3.    Serotonin

Serotonin is a monoamine released by blood platelets. It is synthesised in the CNS and released when the brainstem is stimulated by sensory input. Peripherally, serotonin is an algogenic agent and relates specially to vascular pain syndromes. In the CNS, it is an important element in the endogenous anti-nociceptive mechanism. The activation of serotoninergic pathways in the brainstem by tricyclic antidepressants yields paralysing analgesic effect along with action in depressive states.

4.    Substance P

The substance P is a polypeptide composed of 11 amino acid residues. It is released at the central terminals of primary nociceptive neurons and act as a transport system, being found in distal terminals as well. Centrally, it acts as an excitatory neurotransmitter for nociceptive impulses. It is released from spinal cord cells by stimulation of A- and C afferent fibres, and excites neurons in the dorsal horns that are activated by noxious stimuli. Its modulating action in pain is rapid and short-lived.

5.    Histamine

Histamine is a vasoactive amine that derives from the amino acid histidine. It is a vasodilator and increases the permeability of all vessels. It has been postulated that it also serves as a CNS neurotransmitter.

6.    Other agents

A number of other substances are said to be algogenic. These include potassium and acetylcholine as well as a variety of extraneous toxic substances. Extrinsic algogenic substances are strong irritants which induce pain when applied to skin and mucous membrane or when injected into the body e. g. strong acids, alkalies, organic solvents, certain drugs (thiopentone).


Pain pathways

Pain sensation from the face and the mouth is mediated centrally by way of the afferent primary neurons that pass through the posterior roots of the fifth (trigeminal), seventh (facial), ninth (glossopharyngeal) and tenth (vagus) cranial nerves and the first, second and third cervical spinal nerves. To some extent, it is also by way of visceral afferents that descend through the cervical sympathetic chain to pass through the posterior roots of the upper thoracic spinal nerves.

All the pain fibres of the maxillofacial region terminate in the nucleus caudalis, which is the lower caudal portion of the massive trigeminal spinal tract nucleus. The initial synapses occur in the substantia gelatinosa of the nucleus caudalis, where the secondary medullary (second-order) neurons begin and considerable convergence takes place.

The secondary medullary trigeminal neuronal fibres project to the thalamus, approximately half crossing the midline before they do so. In the thalamus, they terminate in several nuclei and synapse occurs with third order neurons. The tertiary neurons, after greater convergence, project to the cerebral cortex. (See Plate I)

Primary pathways

When the fibres from the sensory root of the trigeminal nerves enter the brain, they pass through three sensory nuclei – the mesencephalic nucleus (uppermost), the principal nucleus and the spinal nucleus (lowest), the latter two being continuous with each other.

The mesencephalic nucleus receives fibres carrying proprioceptive impulses from the muscles of mastication, the tongue, the orbital muscles and the periodontal membrane. Many fibres from all the branches dichotomise to form ascending and descending branches. The former goes to the principal nucleus carrying impulses mediating touch and pressure. The descending branch also carries impulses mediating touch and pressure, and runs with fibres that have not dichotomised, some of which carry impulses mediating pain and temperature. Together, they form a distinct bundle called the spinal tract of the trigeminal nerve, which extends to the lower end of the medulla oblongata. Fibres from all three segments descend as far as the 2nd and 3rd cervical segments. As they descend, the fibres pass to the spinal nucleus which lies medially. The fibres mediating touch and pressure terminate in the upper part of the nucleus.

In the spinal tract, nerve fibres derived from the mandibular division runs postero-medially, those from ophthalmic division run laterally and the maxillary division fibres lie in between. This arrangement is constant, and allows for selective cutting in patients of facial neuralgias. The fibres of the middle part of the face terminate at the highest levels. This ‘onion peel’ distribution of innervation applies to all three divisions of the trigeminal nerve.

The spinal nucleus is further divided into three zones

  1. The nucleus oralis (uppermost – rostrally)
  2. The nucleus interpolaris (intermediate)
  3. The nucleus caudalis (lowest-caudally)

The nucleus caudalis is the most significant for the arrival of impulses mediating pain. In general, the larger nerve fibres of the trigeminal nerve go to the principal sensory nucleus and the nucleus oralis, the smaller fibres going to the nucleus caudalis. This seems to apply also to the fibres of the dental polyp.

In the nucleus caudalis, the fibres end in the substantia gelatinosa and in the more superficial marginal layer. The marginal layer contains projection neurons. The substantia gelatinosa contains two kinds of interneurons, one of which is excitatory and the other inhibitory. Thus, the morphology is similar to that of the dorsal horn of spinal cord. Although it is known that the principal nucleus is homologous with dorsal column nuclei, and the nucleus caudalis with the spinal cord dorsal horn, the functional position of nucleus oralis and interpolaris have not been established.

Secondary pathways

The second order neurons of the trigeminal system form three different pathways that ascend in the brain. Fibres from the principal sensory nucleus form the trigeminal leminiscus which crosses the midline to travel with the medial leminiscus, which has already crossed at a lower level. Together they go to the thalamus and end somatotopically in the ventro-posterior position.

The other two secondary pathways take origin in the spinal trigeminal nucleus. One of them, the neospinothalamic tract is assumed to arise from the cells which receive the descending branches of the dichotomised primary trigeminal axons. The cells of origin of this tract receive mechanoreceptive information and also thermal and pricking pain receptors.

The third secondary pathway from the spinal trigeminal nucleus arises from cells whose input consists of small myelinated and non-myelinated fibres in the trigeminal nerve coming from high threshold mechanoreceptors and thermoreception. Their output is either to the lateral reticular formation or deeper to the medial reticular formation, which in turn, transmits to the intralaminar nuclei of the thalamus.

Tertiary pathways

Neural impulses mediating touch and pressure are conveyed from the thalamus via the posterior limb of the internal capsule, where they occupy a very compact area, to the post-central gyrus of the cerebral cortex.

Representation at the cortex

The structures of the mouth and the face, including teeth, are represented at the cortex for touch and pressure in the post-central gyrus, the primary somatic area. The representation of the face is not inverted as often supposed.


Theories of pain

It has been suggested that pain occurs only when the rate of tissue damage is sufficiently rapid, the damage being done particularly to the pain nerve endings. However, traumatically caused pain is usually very rapid but does not necessarily evoke pain, at least some considerable time afterwards.

Various theories have been put forward on how nerve impulses can give rise to sensation of pain. There is not yet a generally accepted theory.

Intensity theory

According to this view, pain is produced when any sensory nerve is stimulated beyond a certain level. This is true of nerves mediating the sensation of touch when stimulated to excessive degree. In other words, pain is supposed to be non-specific sensation, and depends only on high intensity stimulation. Thus application of heat is pleasant, but excessive heat causes burning.

The theory does not take into account that the more intense thermal stimulus excites additional high threshold fibres. Another example against this theory is the case of trigeminal neuralgia, where the patient suffers excruciating pain from a stimulus no greater than a gentle touch applied to the trigger zone.

Although the theory is not accepted, it remains true that the intensity in stimulation is a factor in causing pain.

Specificity theory

This theory states that pain is a specific modality equivalent to vision and hearing, just as there are Meissner’s corpuscles for the sensation of touch, Ruffini’s end organs for the sensation of warmth etc. Associated with the peripheral pain receptors, there are pain nerves and even a specific central apparatus, the pain centre, in the thalamus.

The nerves concerned are small fibres of the A-d and C groups which pass into the spinal cord, many going to the spinothalamic tract, and then conveyed to the thalamus. In terms of this theory, there is a direct line from the receptor to the brain, and the requisite stimulus at the receptor is necessarily followed by pain sensation.

Specialisation is known to exist in the nervous system, and there are well known tracts in the CNS. It is accepted that C-fibres convey impulses mediating pain. But some C fibres respond to mechanical stimuli of only a few mgs of skin pressure which does not cause pain i.e. they are not specific for nociceptive stimuli. Further, this theory fails to explain why a person who has suffered injury during an exciting game fails to appreciate the pain immediately.

The concept of a pain centre in the brain is incorrect (Melzack and Wall–1968, Zimmermann-1979). Surgical disruption of nerves (trigeminal tractotomy) may fail to abolish pain. This is because the direct line implied by this theory is bypassed and pain may be conveyed to the higher centres through the reticular activating system. Finally, even the concept of specific nerve endings is no longer tenable. No cutaneous receptor has absolute specificity though they have a high degree of selective sensitivity.

Protopathic and epicritic theory

Head and Rowers (1908) postulated the existence of two groups of cutaneous sensory nerves extending from the periphery to the CNS, the protopathic and epicritic systems. The protopathic system is primitive, yielding diffuse impressions of pain, including extremes of temperature and is ungraded. The epicritic system is concerned with touch, discrimination and small changes in temperature and is phylogenetically a more recent acquisition.

While pointing out the difficulties of the theory, Sinclaire (1967) argued that the perceived distinction between these ‘systems’ could be attributable to the spinothamic and lemniscal systems. Marnford and Bowsher (1976) felt it useful to retain the term ‘protopathic’ for the ill-defined sensory experiences evoked by the activation of small primary afferent fibres in the absence of activity in the A-d and C groups.

Pattern theory

Essentially this theory is that pain sensation depends upon the spacio-temporal pattern of nerve impulses reaching the brain. According to Weddell (1962), warmth, cold and pain are words used to describe reproducible spacio-temporal patterns or codes of neural activity evoked from the skin by changes in its environment.

One form of this theory is based on the view that all or nearly all receptors are essentially non-specialised. But their qualities are important, including the thresholds of excitation, adaptation rates, response changes and the distribution of branches of nerve fibres. These qualities differ considerably – some are sensitive to heat, some to pressure – and they have different adaptation rates and different stimulus strength-response curves, different sizes and shapes of receptor fields etc. Weddell (1966) did not completely deny the specificity theory. However, he stresses the danger of correlating the evocation of a particular sensation with the activity produced in the cutaneous nerve fibres by stimuli having specific physical attributes.

Gate Control theory

The Gate control theory was proposed by Melzack and Wall in 1965 and subsequently expanded by Casey and Melzack.

According to them, pain is not due to neural activity that resides exclusively in those pathways traditionally considered specific for pain but rather it is the result of activity in several interacting neural systems each with its own specialised function.  In the spinal cord impulses evoked by peripheral stimulation are transmitted to three systems.

1)       The cells in the substantia gelatinosa

2)      The dorsal column fibers that project toward the brain.

3)      The first central transmission (T) cells in the dorsal horn.

The substantia gelatinosa function as a gate-control system that modulates (facilitates or inhibits) the efferent patterns before they influence the T cells.   The afferent pattern in the dorsal column system act, in part at least, as a central control trigger that activates selective brain processes to influence the modulating properties of the gate-control system.

The T cells activate the neural mechanism comprising the action system responsible for perception of a response to pain. The signal that triggers the action system occurs when the output of the T cells reaches or exceeds the critical level. This critical level of firing is determined by the afferent barrage that impinges on the T cells and has already undergone modulation by substantia gelatinosa activity. This is determined by a relative balance of activity between large and small peripheral fibres.

According to Melzack and Wall, the dorsal column and dorsolateral projection pathways act as a central control trigger. They carry precise information about the nature and location of the stimulus and conduct so rapidly that they may not only set the receptivity of cortical neurons for subsequent afferent volleys but may by way of descending fibres influence the sensory input at the gate-control system and various other levels. This rapid transmission makes it possible for the brain to identify, evaluate, localise and selectively modulate the sensory input before the action system is activated.

There is general agreement that the large cutaneous A fibres are effective in inhibiting spinal sensory input from both large and small diameter cutaneous fibres.

Casey and Melzack have expanded the theory by taking into account more recent physiologic and behavioural studies the further emphasise the motivational affective and cognitive aspects of the pain experience.  These pertain to neural systems beyond the gauge and involve interaction of the neospinothalamic and paleospinothalamic projecting systems and neocortical processes.  All three forms of activity influence motor mechanisms responsible for the complex pattern of evert responses that characterise pain.

Despite its deficiencies the Melzack-Wall-Casey model of pain has proved to be one of the most important development in this field.  It is the most comprehensive formulation of pain that might provide a theoretical basis for some of the pathologic states.

 

 

Pain perception

Pain perception depends not only on the integrity of the peripheral and central nervous pathways but also on the peripheral pain receptors and the patient’s own psyche. Ethnic and cultural factors may influence a person’s reaction to pain and may colour the description of it.  The general health, tiredness or nutritional status a person may also have profound effect on how a person reacts to discomfort.

Everyone has experienced the phenomenon that when the mind is fully occupied with other things, such pains are tolerable but for example in the long reaches of the night when the mind is free to dwell on a pain it may become intolerable.  All of these matters must be kept in mind when a pain history is being taken and this highly personal reaction often makes a diagnosis very difficult.  Facial pain is felt to be more severe and produces longer reactions because it seem a more intimate part of one’s personality, whereas the pain felt in the finger can be viewed more objectively.

Factors which are capable of lowering the pain threshold include discomfort, insomnia, fatigue, anxiety, fear, anger, sadness, depression, boredom, mental isolation, social abandonment etc. At the same time, some factors would serve to raise the threshold. They are relief of other symptoms, sleep, sympathy, understanding, companionship, creative activity, relaxation, reduction in anxiety, elevation of mood and drugs like analgesics, anxiolytics and antidepressants.

 

 

Localisation of pain

Localisation of the source of pain is one of the most important aids to diagnosis of disease. It is accurately localised in the skin and mucosa, but the accuracy is lost as the source of pain sinks deep into the body. It may be said that pain is localised primarily to the segments corresponding to the stimulated nerves and that accuracy is superimposed on this segmental pattern. In the skin, the accuracy of localisation of pain appears to be based on the richness of its innervation, the multiple innervation of pain spots and on the associated nervous mechanism for accurate localisation of touch. In deeper structures, innervation is much sparser and there is no other sensory mode to aid in localisation of pain. In these circumstances, pain may be felt on any part of one affected segment. Localisation of pain is believed to be a function of cerebral cortex.

Referred pain from deep structures is that pain which occurs in addition to or in the absence of true visceral or deep somatic pain. It is felt at a site other than that of stimulation, in deep or superficial structures supplied by the same or adjacent neural segments. The pain is most frequently referred to other parts of the same segment but it may spread to adjacent segments. Pain is more commonly referred to the anterior than to the posterior half of the body e.g. angina pectoris, peptic ulcer etc.


Methods of assessing pain

Since pain is a subjective experience that is communicated only through words and behaviours, it is extremely difficult to measure pain. There are several physiological and psychological factors that will influence the intensity of pain perceived. Measuring pain is important for studying pain mechanisms in the laboratory, and to assess treatment outcome. A number of instruments have been developed and tested for their reliability and validity in measuring different aspects of the pain experience.

Quantifying the pain experience

Visual analogue scale

A visual analogue scale is that represents a continuum of a particular experience such as pain. The most common form used for assessing pain is a 10cm line, either horizontal or vertical, with perpendicular stops at the ends. The ends are anchored by labels ‘no pain’ and ‘worst imaginable pain’. Numbers should not be used along the line to ensure a better, less biased distribution of pain ratings. Patients are asked to place a slash mark somewhere along the line to indicate the intensity of their current pain complaint. For scoring purposes, a millimetre ruler is used to measure along the line and obtain a numerical score for the pain ratings.

McGill Pain Questionnaire

The McGill pain questionnaire is a verbal pain scale that uses a vast array of words commonly used to describe a pain experience. Different types of pain, different diseases and disorders, have different qualities of pain. Melzack and Torgerson (1971) categorised the verbal descriptors into classes and subclasses designed to describe different aspects of the pain experience. In addition, ‘affective descriptors’ such as fear and anxiety and evaluative words describing the overall intensity of pain, were included.

The words are listed in 20 different categories. They are arranged in order of magnitude from less intense to most intense, and are grouped according to distinctly different qualities of pain. The patient is asked to circle only one word in each category that applies to them.

Melzack uses this master-list of words to derive quantitative measures of clinical pain that can be treated statistically. It can also detect changes in pain with different treatment modalities.

Psychological assessment

Chronic pain is the most complicated of pain experiences. Determining the emotional, behavioural and environmental factors that perpetuate chronic pain is as essential as establishing the correct physical diagnosis. Traditionally, the systematic assessment of psychosocial difficulties is achieved through a psychological interview and a battery of psychological tests.  The tests designed to assess psychopathology include the Minnesota Multiphasic Personality Inventory (MMPI), the Beck Depression Inventory, and Symptom checklist-90.

The instruments that could be used by the clinician to evaluate the chronic pain patient in a routine clinical setting include the Beck Depression Inventory (BDI -1978) and the Chronic Illness Problem Inventory (CIPI -1984). These consist of questionnaires which are easily administered, self-report and problem-oriented.


Diagnosis of orofacial pain

Every pain has its distinct and pregnant significance if one searches carefully for it. The diagnosis of orofacial pain may prove to be one of the most challenging and frustrating problems faced by the dental practitioner. The various organ that lie within the face, coupled with the great variety of diseases to which they may succumb account for many different types of facial pain. The extreme richness of the nerve supply of the area, perhaps the richest sensory innervation of any part of the body, also accounts for the many subtleties of pain that may be experienced in the face. Pain may arise from the teeth, the periodontium, the jaws, joints, muscles, ligaments, nasal cavity and accessory sinuses, eyes, ears and blood vessels. In some cases, what presents as odontogenic pain may be the first significance of a life threatening disease. Pain arising from disease within the cranial cavity may also be experienced in the face, as may be referred pain from such remote sites as the heart. Cardiac effort pain (angina pectoris) may occasionally be experienced predominantly in the neck or jaw.  It is now well recognised that pain in the face may also be associated with psychiatric disorders such as depression.

CLASSIFICATION OF OROFACIAL PAIN SYNDROMES

  1. Based on the anatomical location where pain is felt.
  2. Head and neck pain – headache

– orofacial pains

– cervical pains

  1. Thoracic pain
  2. Abdominal
  3. Extremity pain
  4. Orofacial pains are classified regionally as:
  5. Cutaneous and mucogingival pains.
  6. Mucosal pains of the pharynx, nose and PNS.
  7. Pains of dental origin.
  8. Pains of the musculoskeletal structures of the mouth and face.
  9. Pains of the visceral structures of the mouth and face.
  10. Pains of the neural structures of the mouth and face.
  11. Chronic face pain syndromes.

Pain syndromes about the mouth and face may be divided by their clinical characteristics into three categories.

  1. Somatic pain: results from noxious stimulation of normal neural structures that innervate body tissues.
  2. Neurogenous pain: is generated within the nervous system itself and is caused by abnormality of the neural structures that innervate body tissues.
  3. Psychogenic pain: results neither from noxious stimulation nor from neural abnormality but from psychic causes.


Management of Patients in Pain

Treatment modalities

  • Cause-related therapy: consists of identification and elimination of aetiologic factors.
  • Sensory stimulation: This is utilising the pain inhibitory affects of stimulating certain afferent neurons.
    • cutaneous
    • transcutaneous
    • percutaneous nerve stimulation.
  • Analgesic blocking: This is the use of local anaesthesia to
    • arrest pain input
    • interrupt cycling
    • resolve myofascial trigger point activity
    • induce sympathetic blockade
  • Physiotherapy: This includes cutaneous, and deep massage, exercises, deep
    heat therapy, trigger point therapy, physical activity to increase “up-time”.
  • Relaxation training: This includes autosedation, biofeedback training and
    occlusal disengagement.
  • Placebo therapy
  • Psychotherapy: This includes counselling, hypnotherapy, and contingency management and formal psychotherapy.
  • Neurosurgery: includes procedures as:
    • peripheral therapy
    • gangliolysis, rhizotomy and decompression
    • trigeminal tractotomy.
  • Medicinal therapy: which includes
    • analgesics
    • anti-inflammatory agents
    • analgesic balms
    • antiherpes agents
    • local anaesthetics
    • anticonvulsants
    • neuroactive drugs
    • tranquillisers and muscle relaxants
    • antidepressants
    • vasoactive agents.
  • Dietary supplements

Pain management as far as somatic pain is concerned applies only to primary sources.  Heterotopic pain whether spontaneous referred pain or evoked secondary hyperalgesia can’t be treated directly.  Only through identification and treatment of the primary source can such pain be managed.


Methods to prevent pain in surgical patients

General anaesthesia

General anaesthesia is a controlled state of unconsciousness accompanied by a partial or complete loss of protective reflexes, including the ability to maintain a patent airway and respond purposefully to physical stimulation or verbal command, produced by a pharmacological method, or a combination thereof. After adequate premedication (sedatives, anxiolytics etc.) and pre-oxygenation (100% oxygen for 3 to 5 minutes), a short acting sedative is administered intravenously. An endotracheal tube is inserted through oral or nasal cavity. Anaesthetic gases like N2O, halothane etc can be administered through the tube to maintain the anaesthesia.

Sedation

Sedation is depressed level of consciousness which may vary from light to deep.

Conscious sedation

Conscious sedation is a minimally depressed level of consciousness that retains the patient’s ability to independently and continuously maintain the airway and to respond appropriately to physical stimulation and verbal command at any time, produced by a pharmacologic or non-pharmacologic method or a combination thereof. The loss of consciousness should be unlikely and the drugs and techniques used should carry a safety wide enough to render the unintended loss of consciousness unlikely.

Common drugs used include diazepam, midazolam, pentobarbital etc. These may be used with or without N2O –O2 supplementation.

Deep sedation

A controlled state of depressed consciousness or unconsciousness from which the patient is not easily aroused, which may be accompanied by a partial or complete loss of protective reflexes including the inability to independently maintain a patent airway and respond purposefully to physical stimulation or verbal command, produced by a pharmacologic or non-pharmacologic method or a combination thereof.

The combination of intravenous midazolam, fentanyl, N2O –O2, and small increments of methohexital are widely used for deep sedation. Intramuscular ketamine produces excellent deep sedation for approximately 30 minutes.

Local anaesthesia

Local anaesthesia is the use of a potent drug to produce temporary loss of all modalities of sensation in a limited region of the body. Local analgesia is the loss of sensation of pain. This can be achieved by surface application or infiltration and regional injection of drugs. A local anaesthetic drug is placed near the sensory nerves so as to temporarily prevent the conduction of pain impulses to the brain.

Surface analgesia may be achieved by topical application of the analgesic drugs, the main methods of application being pastes, solutions, sprays, jet injectors, lozenges and mouthwashes. The injectable local anaesthetics are used either as an infiltration or as a regional block.

Acupuncture analgesia

Acupuncture analgesia is thought to have originated in China about 3000 or more years ago. It makes use of acupuncture needles inserted at various sites on the body based on the ancient meridian theory. The needles are twirled at 100-200 cycles/min, or instead stimulated by an electrical acupuncture machine which uses a current of about 3mA at the frequency ranging from 300-3000 cycles/minutes. The mechanism of action is believed to be the excitation of A-d fibres leading to the production of endorphins.

Hypnotism

Hypnotism induces a trance-like state in which the patient’s attention is focussed on the operator so that awareness of other stimuli such as pain is markedly reduced, or not felt at all. This is method is of use only in susceptible and co-operative patients. Also, it may initially be time-consuming.

Audio-analgesia

Described by Gardner and Licklider (1959), this method uses loud sounds to produce insensitivity to pain in some patients. The patient wears stereophonic earphones and controls the volume and type of sound. He increases the volume of sound when the pain becomes uncomfortable. The explanations to the success of this method are relaxation, need for concentration, stimulation of other sensory tracts etc.

Electric anaesthesia (anelectrotonus)

In 1950, Suzuki described a method of blocking nerve conduction in the peripheral part of the pain pathway by use of a direct electric current. The physiological basis of this is that a pain impulse is accompanied by a negative potential, and depolarisation of the nerve fibre is prevented by introducing as positive potential due to a direct electrical current. The best results with this technique are obtained in children less than 10 years of age.

Anaesthesia by cold air

When a part of the body becomes sufficiently cold, pain sensation is abolished due to the inability of nerve fibres to conduct action potentials at low temperatures. This principle of lowering the temperature of the tissues to achieve anaesthesia is used in clinical situation by spraying on a volatile material such as ethyl chloride. As it evaporates, it removes heat from the tissues due to its latent heat of evaporation, and thus chills them.

Conclusion

A surgeon should be aware of the physiologic and psychological aspects of pain and anxiety as it applies to the patient. There is a vast array of diseases that manifest with painful symptoms clinically. Adequate clinical assessment and diagnosis are the keys to successfully manage such conditions.

Pain caused by surgical procedures is an anathema to the patients. The surgeon should be aware of the different methods to alleviate the sufferings of the patient and should apply them to situations as necessary.


References

 

 

  1. Samson Wright’s Applied Physiology.
  2. Local analgesia in dentistry. 3rd edition. DH Roberts and JH Sowray. 1987.
  3. Miller’s Anaesthesia Vol. I
  4. Monheim’s Local Anaesthesia and Pain Control in Dental Practice.
  5. Review of medical physiology. 14th edition. WF Ganong. 1989.
  6. Orofacial pain –classification, diagnosis and management – Welden E Bell
  7. Dental pain. Dental Clinics of North America. October 1987.
  8. Differential diagnosis and management of craniofacial pain. B Jaeger. In Endodontics. 4th edition. JI Ingle, LK Bakland (ed)
  9. Management of Pain and Anxiety. J Weaver. In Principles of Oral and Maxillofacial Surgery (ed) LJ Peterson, RD Marciani. AT Indresano. 1997.
  10. Office anaesthesia evaluation manual. 3rd edition. American Association of Oral and Maxillofacial Surgeons. 1986.
  11. Burcket’s Oral Medicine: diagnosis and treatment. 9th edition. (eds) MA Lynch, VJ Brightman, MS Greenberg. 1994.