Spring ushers in new blossoms, warmer temperatures, and the start of pool season. To get maximum enjoyment from your pool, it’s important to keep it clean. An automatic cleaner (also referred to as a pool vacuum) allows you to spend more time splashing around in your pool rather than on the deck cleaning it. So before the pool season gets underway, make sure your pool cleaner is working or consider purchasing a newer model to keep your pool’s surfaces thoroughly clean.
If you’re in the market to buy a new pool cleaner, there are three questions you should consider when deciding which pool cleaner is best for you:
What kind of pool do you have?
What type of dirt and debris do you have?
How much maintenance is involved?
How to Choose a Pool Cleaner: Three Main Pool Cleaner Options
Pressure Cleaners
Pressure-side cleaners connect to the pool via a dedicated return line and may require a separate booster pump to operate. Debris is captured in an attached filter bag — keeping it out of your pool’s filtration system and prolonging the life of your pool filter. If your pool system was built with the appropriate plumbing to support a pressure-side cleaner, then a pressure cleaner would be an ideal choice for you.
Good for general cleaning, pressure-side cleaners feature a large throat for exceptional removal of big debris such as leaves, twigs, acorns and pebbles. Plus, pressure cleaners move around distributing clean, and heated water throughout the pool, reducing cold spots. Overall, pressure cleaners are easy to use and simply require routine emptying of the debris bag to maintain effective performance.
As the creators of the first three-wheeled pressure cleaner on the market over 40 years ago, Polaris continues to lead this category with top-performing cleaners like the Polaris Quattro Sport, which capably collects both fine and large debris with its innovative Dual-Stage Filtration and actively scrubs away stuck-on debris with its unique brush design.
Suction Cleaners
Attached through the skimmer or dedicated suction line, a suction-side pool cleaner sucks up debris, capturing it in the leaf catcher, skimmer basket, or pump filter basket. Designed for efficiency, suction cleaners operate quietly while your pool system is running (when swimmers are out of the water).
Suction cleaners do a fantastic job at collecting fine debris like sand and algae. Some models, like the Zodiac MX8™ Elite even feature cyclonic scrubbing brushes to remove stuck-on debris from the floors, walls and tile line. With just a bit of maintenance to empty the skimmer and pump filter basket regularly, a suction cleaner may be the right choice for you.
Robotic Cleaners
Unlike pressure and suction cleaners, robotic cleaners aren’t powered by your pool’s filtration system and can be used with any type of in-ground pool. Just plug it in to an outdoor GFCI (ground fault circuit interrupter) electrical outlet, place it in the pool, and the robotic cleaner goes to work drawing in everything from medium debris to fine particles — like algae, pollen, sand, leaves and pebbles — and collecting it in an easy-to-clean internal canister.
Some robotic cleaners even provide premium features like custom cleaning cycles while maximizing energy efficiency and pool cleaning coverage for quicker cleaning times. A robotic cleaner cleans for just pennies a day, consuming less energy than other types of cleaners, however, they do require a slightly higher level of hands-on interaction — needing to be removed from the pool after each use and regular debris removal from the canister.
Popular models by Polaris® include the 7240 Sport, which offers lightweight handling, Cyclonic Vacuum technology that captures debris without losing suction throughout the cleaning cycle, and features an Easy Clean Filter Canister with a transparent lid so you can see when it’s full. A more advanced option is the Polaris ALPHA iQ+, a best-in-class 4-wheel-drive robotic cleaner with SMART cleaning technologies that learn your pool and that can be controlled by the intuitive iAquaLink™ mobile app via a WiFi connection — allowing you to clean, monitor, schedule, and troubleshoot anytime, anywhere.
Whichever type of automatic pool cleaner you wind up with, start using it when you first open the pool and stick to a routine cleaning schedule to ensure that your pool water remains clear and swim-ready. Think of it as being proactive and preventing potential problems.
Coke vs. cola, spa vs. hot tub: these are among the many soft lines in the sand that we use to describe similar-yet-distinctive things. And like how “soda” and “pop” can mean both Coke and Pepsi, people use the words “spa,” “hot tub” and “Jacuzzis®” interchangeably.
So what sets them apart? Which word describes what you’re looking for best? Read on to learn the difference between a spa and a hot tub, and which one’s a better fit for your backyard.
The Real Question: Build or Buy?
Both hot tubs and spas are hydrotherapeutic, using heat and water jets to create relaxing, pleasurable experiences. The biggest difference between a spa and a hot tub is in their construction: spas are built on site, whereas hot tubs are bought as prefabricated units.
Spas
These in-ground units are typically built as permanent improvements to existing backyard pools. Since they’re constructed from scratch in your backyard—from excavation to steel/rebar installation, to pouring the spa surface and applying a finish—the building process of a spa connected to a new pool will typically take several weeks, depending on the timeline for the pool build. With these custom builds, more space is required in a backyard for the in-ground spa, the connection pool and the equipment pad.
Because they’re built specifically for a homeowner, spas give people the freedom and flexibility to customize the design tailored to their preferred aesthetic. From shape and size to LED lighting, to customized jet placement, overflow edges and other custom design elements, spas can be built to owners’ exact specifications. And, because they’re built in conjunction with a pool, spas use the same equipment pad as an in-ground pool, including the pool heater, pump, and filtration systems.
Another differentiator is the intended purpose of a spa. It’s usually built as a complementary feature to further enhance the enjoyment of a residential pool. Swimmers can easily hop from the pool right into a connected spa to warm up and relax after a swim.
Hot tubs
Since these units are prefabricated, all homeowners need to do is buy and install them. One could easily go to a nearby pool supply store, buy a hot tub unit, and have it installed in their backyard that same day. Because of their prefab nature, hot tubs are by definition above-ground and freestanding. All hot tub components are built into the hot tub “cabinet” or housing, including the plumbing and electrical systems. This allows convenience at a lower cost and takes up less space, but does sacrifice durability and customization.
Since hot tubs are independent from pools and can typically be added at less expense than a pool, they are especially popular with homeowners who are not yet ready to invest in building an in-ground pool or who may not have the space for a pool. It isn’t uncommon for a hot tub to be the main feature for backyard entertainment.
But what about Jacuzzis? Allow us to explain.
Wait, then What’s a Jacuzzi®?
Saying “Jacuzzi vs. hot tub” is a bit redundant. Jacuzzi is to a hot tub as Kleenex is to tissue.
Put simply, a Jacuzzi is a brand of hot tub. The Jacuzzi brand first paved the way for the home hydrotherapy market and delivered it to the masses.
Here’s a little history for you: Claudio Jacuzzi adapted his family’s agricultural water pump technology to fit a residential-sized tub to treat his child’s juvenile rheumatoid arthritis. The hot water and jet streams soothed his child’s aching joints. From there, he developed it into a product for sale. Given the opportunity to place the Jacuzzi-brand hot tubs as a prize on the 1950s television show Queen for a Day, the hot tub entered the American cultural lexicon as a symbol of comfort and luxury.
Today, there are many other brands of hot tubs, although in conversation people often refer to any hot tub as a “Jacuzzi.”
What Fits You Best?
So, how do you decide between a spa vs. hot tub? It all comes down to your lifestyle. Whether you prefer a permanent spa that complements your in-ground pool or a less expensive, separate above-ground system offering the same hydrotherapy benefits, both options will help enhance your backyard.
Water balance means the inflows to any water system or area are equal to its outflows plus the change in storage during a time interval. In hydrology, a water balance equation can be used to describe the flow of water in and out of a system. A system can be one of several hydrological or water domains, such as a column of soil, a drainage basin, an irrigation area or a city. Water balance can also refer to the ways in which an organism maintains water in dry or hot conditions. It is often discussed in reference to plants or arthropods, which have a variety of water retention mechanisms, including a lipid waxy coating that has limited permeability.
Regulation of Water Intake
Fluid can enter the body as preformed water, ingested food and drink, and, to a lesser extent, as metabolic water.
Key Points
A constant supply of water is needed to replenish the fluids lost through normal physiological activities, such as respiration, sweating, and urination.
Thirst is a sensation created by the hypothalamus that drives organisms to ingest water.
Increased osmolarity in the blood acts on osmoreceptors that either stimulate the hypothalamus directly or cause the release of angiotensin II to stimulate the hypothalamus to cause thirst.
The renin-angiotensin system increases thirst as a way to increase blood volume. It is activated by high plasma osmolarity, low blood volume, low blood pressure, and stimulation of the sympathetic nervous system.
Key Terms
thirst: The sensation that drives organisms to ingest water. It is considered a basic survival instinct.
osmoreceptors: Sensory receptors that are primarily found in the hypothalamus or macula densa that detect changes in the solute concentration of blood.
Water Intake
Fluid can enter the body as preformed water, ingested food and drink, and, to a lesser extent, as metabolic water that is produced as a by-product of aerobic respiration and dehydration synthesis. A constant supply is needed to replenish the fluids lost through normal physiological activities, such as respiration, sweating, and urination.
Water generated from the biochemical metabolism of nutrients provides a significant proportion of the daily water requirements for some arthropods and desert animals, but it provides only a small fraction of a human’s necessary intake. In the normal resting state, the input of water through ingested fluids is approximately 2500 ml/day.
Body water homeostasis is regulated mainly through ingested fluids, which, in turn, depends on thirst. Thirst is the basic instinct or urge that drives an organism to ingest water.
Thirst is a sensation created by the hypothalamus, the thirst center of the human body. Thirst is an important component of blood volume regulation, which is slowly regulated by homeostasis.
Hypothalamus-Mediated Thirst
An osmoreceptor is a sensory receptor that detects changes in osmotic pressure and is primarily found in the hypothalamus of most homeothermic organisms. Osmoreceptors detect changes in plasma osmolarity (that is, the concentration of solutes dissolved in the blood).
When the osmolarity of blood changes (it is more or less dilute), water diffusion into and out of the osmoreceptor cells changes. That is, the cells expand when the blood plasma is more dilute and contract with a higher concentration.
When the osmoreceptors detect high plasma osmolarity (often a sign of a low blood volume), they send signals to the hypothalamus, which creates the biological sensation of thirst. Osmoreceptors also stimulate vasopressin (ADH) secretion, which starts the events that will reduce plasma osmolality to normal levels.
The hypothalamus: The hypothalamus is the thirst center of the human body.
Renin-Angiotensin System-Mediated Thirst
Another way through which thirst is induced is through angiotensin II, one of the hormones involved in the renin-angiotensin system. The renin-angiotensin system is a complex homeostatic pathway that deals with blood volume as a whole, as well as plasma osmolality and blood pressure.
The macula densa cells in the walls of the ascending loop of Henle of the nephron is another type of osmoreceptor; however, it stimulates the juxtaglomerular apparatus (JGA) instead of the hypothalamus. When the macula densa is stimulated by high osmolarity, The JGA releases renin into the bloodstream, which cleaves angiotensinogen into angiotensin I. Angiotensin I is converted into angiotensin II by ACE in the lungs. ACE is a hormone that has many functions.
Angiotensin II acts on the hypothalamus to cause the sensation of thirst. It also causes vasoconstriction, and the release of aldosterone to cause increased water reabsorption in a mechanism that is very similar to that of ADH.
Note that the renin-angiotensin system, and thus thirst, can be caused by other stimuli besides increased plasma osmolarity or a decrease in blood volume. For example, stimulation of the sympathetic nervous system and low blood pressure in the kidneys (decreased GFR) will stimulate the renin-angiotensin system and cause an increase in thirst.
Regulation of Water Output
Fluid can leave the body in three ways: urination, excretion (feces), and perspiration (sweating).
Key Points
The majority of fluid output occurs from urination. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air.
The body’s homeostatic control mechanisms ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (antidiuretic hormone, also known as vasopressin ) and aldosterone play a major role in this.
If the body is becoming fluid deficient, increased plasma osmolarity is sensed by the osmoreceptors. This results in an increase in the secretion of ADH that causes fluid to be retained by the kidneys and urine output to be reduced.
Aldosterone is the major end-product of the renin-angiotensin system and increases the expression of ATPase pumps in the nephron that causes an increase in water reabsorption through sodium cotransport.
ADH increases water reabsorption by increasing the nephron’s permeability to water, while aldosterone works by increasing the reabsorption of both sodium and water.
Key Terms
osmoreceptors: Sensory receptors, primarily found in the hypothalamus, that detect changes in plasma osmolarity and contribute to the fluid-balance regulation in the body.
anti-diuretic hormone: A neurohypophysial hormone found in most mammals that is responsible for increasing water absorption in the collecting ducts of the kidney nephrons.
aldosterone: A corticoid hormone that is secreted by the adrenal cortex that regulates the balance of sodium and potassium and thus the water-balance levels in the body.
Water Output
Fluid can leave the body in three ways:
Urination
Excretion (feces)
Perspiration (sweating)
The majority of fluid output occurs from urination, at approximately 1500 ml/day (approximately 1.59 qt/day) in a normal adult at resting state. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air; however, these fluid losses are considered to be very minor.
The body’s homeostatic control mechanisms maintain a constant internal environment to ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (anti-diuretic hormone, also known as vasopressin) and aldosterone, a hormone created by the renin-angiotensin system, play a major role in this balance.
If the body is becoming fluid deficient, there will be an increase in the secretion of these hormones that causes water to be retained by the kidneys through increased tubular reabsorption and urine output to be reduced. Conversely, if fluid levels are excessive, the secretion of these hormones is suppressed and results in less retention of fluid by the kidneys and a subsequent increase in the volume of urine produced, due to reduced fluid retention.
ADH Feedback
When blood volume becomes too low, plasma osmolarity will increase due to a higher concentration of solutes per volume of water. Osmoreceptors in the hypothalamus detect the increased plasma osmolarity and stimulate the posterior pituitary gland to secrete ADH.
ADH causes the walls of the distal convoluted tubule and collecting duct to become permeable to water—this drastically increases the amount of water that is reabsorbed during tubular reabsorption. ADH also has a vasoconstrictive effect in the cardiovascular system, which makes it one of the most important compensatory mechanisms during hypovolemic shock (shock from excessive fluid loss or bleeding).
Aldosterone Feedback
Aldosterone is a steroid hormone (corticoid) produced at the end of the renin-angiotensin system. To review the renin-angiotensin system, low blood volume activates the juxtaglomerular apparatus in a variety of ways to make it secrete renin. Renin cleaves angiotensin I from the liver-produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increased thirst) but it also causes the release of aldosterone from the adrenal cortex.
Aldosterone has a number of effects that are involved in the regulation of water output. It acts on mineral corticoid receptors in the epithelial cells of the distal convoluted tubule and collecting duct to increase their expression of Na+/K+ ATPase pumps and to activate those pumps. This causes greatly increased reabsorption of sodium and water (which follows sodium osmotically by cotransport), while causing the secretion of potassium into the urine.
Aldosterone increases water reabsorption; however, it involves an exchange of sodium and potassium that ADH absorption regulation does not involve. Aldosterone will also cause a similar ion-balancing effect in the colon and salivary glands as well.
A schematic diagram of the renin-angiotensin system: Overview of the renin-angiotensin system that regulates blood pressure and plasma osmolality.
Nitrogenous Waste in Terrestrial Animals: The Urea Cycle
P is precipitation is streamflow is evapotranspiration
ΔS is the change in storage (in soil or the bedrock/groundwater)
This equation uses the principles of conservation of mass in a closed system, whereby any water entering a system (via precipitation), must be transferred into either evaporation, transpiration, surface runoff (eventually reaching the channel and leaving in the form of river discharge), or stored in the ground. This equation requires the system to be closed, and where it isn’t (for example when surface runoff contributes to a different basin), this must be taken into account.
Extensive water balances are discussed in agricultural hydrology.
A water balance can be used to help manage water supply and predict where there may be water shortages. It is also used in irrigation, runoff assessment (e.g. through the RainOff model [rx]), flood control, and pollution control. Further, it is used in the design of subsurface drainage systems which may be horizontal (i.e. using pipes, tile drains, or ditches) or vertical (drainage by wells).[rx] To estimate the drainage requirement, the use of a hydrogeological water balance and a groundwater model (e.g. SahysMod[rx]) may be instrumental.
The water balance can be illustrated using a water balance graph which plots levels of precipitation and evapotranspiration often on a monthly scale.
Several monthly water balance models had been developed for several conditions and purposes. Monthly water balance models had been studied since the 1940s.[rx]
Water Balance of a System
“Making water available for its many uses and users requires tools and institutions to transform it from a natural resource to one providing services”.[rx] This means that there are two types of water systems: Water Resource System (WRS) and Water Use System (WUS).
A WRS, such as a river, an aquifer, or a lake, must obey water balance. For example, the volume of water that goes into an aquifer must be equal to the amount that leaves it plus its change in storage. Under various drivers, such as climate change, population increase, and bad management, water storage of many WRS is decreasing, say per decade. This means that the volume of water in a WRS decreased after a decade, i.e., the inflow was less than outflow during that time interval.[rx]
In general, a WUS is a water construct of a user, such as a city, an industry, an irrigation zone, or a region, and not a geographic area. The schematic of a WUS shows the inflows and the outflows. For a WUS, change in storage is negligible (relative to its inflow) under a proper time interval, hence water balance becomes inflow equal to outflow with nine Water Path Types (WPT):[rx]
A typical schematic of a Water Use System (WUS) with its fixed nine Water Path Types
{\displaystyle VA+OS+PP=ET+NR+RF+RP}
Of course, instead of a river, it could be an aquifer that supplies water to a WUS as the main source. Let us briefly examine an urban water supply on an annual basis as a simplified example. It has negligible ET and PP (WUS is a piped network), has some limited amount of water from groundwater (OS), has return flow to the main source (RF) after passing through a Wastewater Treatment Plant, and RP type has various Water Path Instances (WPI), such as leakage, and water is taken to irrigate green zones. Considering that the annual change in storage of an urban area is negligible, the water balance equation becomes
Urea, a nitrogenous waste material, is the end product excreted in urine when ammonia is metabolized by animals, such as mammals.
Key Points
Ureotelic animals, which includes mammals, produce urea as the main nitrogenous waste material.
2 NH3 + CO2 + 3 ATP + H2O → H2N-CO-NH2 + 2 ADP + 4 Pi + AMP is the chemical reaction by which toxic ammonia is converted to urea.
The urea cycle involves the multi-step conversion (carried out by five different enzymes ) of the amino acid L- ornithine into different intermediates before being regenerated.
Key Terms
ureotelic: animals that secrete urea as the primary nitrogenous waste material
ornithine: an amino acid, which acts as an intermediate in the biosynthesis of urea
urea: a water-soluble organic compound, CO(NH2)2, formed by the metabolism of proteins and excreted in the urine
Nitrogenous Waste in Terrestrial Animals: The Urea Cycle
Mammals, including humans, are the primary producers of urea. Because they secrete urea as the primary nitrogenous waste product, they are called ureotelic animals. Urea serves an important role in the metabolism of nitrogen-containing compounds by animals. It is the main nitrogen-containing substance in the urine of mammals. Urea is a colorless, odorless solid, highly soluble in water, and practically non-toxic. Dissolved in water, it is neither acidic nor alkaline. The body uses it in many processes, the most notable one being nitrogen excretion. Urea is widely used in fertilizers as a convenient source of nitrogen. It is also an important raw material for the chemical industry.
Apart from mammals, urea is also found in the urine of amphibians, as well as some fish. Interestingly, tadpoles excrete ammonia but shift to urea production during metamorphosis. In humans, apart from being a carrier of waste nitrogen, urea also plays a role in the countercurrent exchange system of the nephrons, which allows for the re-absorption of water and critical ions from the excreted urine. This mechanism, controlled by an antidiuretic hormone, allows the body to create hyperosmotic urine, which has a higher concentration of dissolved substances than the blood plasma. This mechanism is important to prevent the loss of water, maintain blood pressure, and maintain a suitable concentration of sodium ions in the blood plasmas.
The urea cycle is the primary mechanism by which mammals convert ammonia to urea. Urea is made in the liver and excreted in the urine. The overall chemical reaction by which ammonia is converted to urea is 2 NH3 (ammonia) + CO2 + 3 ATP + H2O → H2N-CO-NH2 (urea) + 2 ADP + 4 Pi + AMP.
The urea cycle utilizes five intermediate steps, catalyzed by five different enzymes, to convert ammonia to urea. The amino acid L-ornithine is converted into different intermediates before being regenerated at the end of the urea cycle. Hence, the urea cycle is also referred to as the ornithine cycle. The enzyme ornithine transcarbamylase catalyzes a key step in the urea cycle. Its deficiency can lead to the accumulation of toxic levels of ammonia in the body. The first two reactions occur in the mitochondria, while the last three reactions occur in the cytosol.
Urea Cycle: The urea cycle converts ammonia to urea in five steps that include the catalyzation of five different enzymes.
Water Balance Disorders
Dehydration is the excessive loss of body fluid.
Key Points
There are three types of dehydration: hypotonic or hyponatremic, hypertonic or hypernatremic, and isotonic or hyponatremic.
Hypotonic dehydration is primarily a loss of electrolytes, sodium in particular.
Hypertonic dehydration is primarily a loss of water.
Isotonic dehydration is an equal loss of water and electrolytes.
Hypovolemia is a loss of blood volume and may cause hypovolemic shock. In humans, the most common type of dehydration by far is isotonic (isonatraemic) dehydration.
Water balance disorders are generally treated by increasing water intake and reducing or stopping fluid loss.
Key Terms
isotonic: When comparing solutions, an isotonic solution has the same osmolarity (ion concentration) as the solution it is being compared to.
plasma: The straw-colored/pale-yellow, liquid component of blood that normally holds the blood cells of whole blood in suspension.
electrolyte: Any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes.
Water Balance Disorders
In physiology and medicine, dehydration (hypohydration) is defined as the excessive loss of body fluid. It is literally the removal of water from an object. However, in physiological terms, it entails a deficiency of fluid within an organism.
Much of the physiological effects of dehydration is due to the changes in ion concentration that may occur as a result of the dehydration. Alternatively, hypovolemia may occur due to loss of blood volume itself.
Dehydration
There are three types of dehydration that differ based on the type of change in ion concentrations:
Hypotonic – primarily a loss of electrolytes, sodium in particular. Hypotonic dehydration causes decreased plasma osmolality.
Hypertonic – primarily a loss of water. Hypertonic dehydration causes increased plasma osmolality.
Isotonic – an equal loss of water and electrolytes. Isotonic dehydration will not change plasma osmolarity, but it will reduce overall plasma volume. Isotonic dehydration is the most common type of dehydration.
Further complications may also occur. In hypotonic dehydration, intravascular water shifts to the extravascular space and exaggerates intravascular volume depletion for a given amount of total body water loss.
Neurological complications can occur in hypotonic and hypertonic states. The former can lead to seizures, while the latter can lead to osmotic cerebral edema upon rapid rehydration.
Hypovolemia
Hypovolemia is specifically a decrease in the volume of blood plasma. Furthermore, hypovolemia defines water deficiency in terms of blood volume rather than the overall water content of the body.
IV fluid and electrolyte administration: Intravenous administration of fluid is one effective treatment of dehydration in humans.
Hypovolemia is a cause of hypovolemic shock. Shock is any condition in which the body’s fluids are unable to properly circulate and oxygenate the major organs of the human body; this causes compensatory mechanisms to activate that cause further bodily harm as the body’s metabolism is maintained for a while longer.
In the case of hypovolemic shock, the tissue metabolism is impaired due to a lack of blood volume and makes it difficult for red blood cells to reach all of the tissues of the body. It is most often caused by severe vomiting, diarrhea, blood loss, or hemorrhage. Other forms of shock with similar symptoms may be due to problems in the heart (cardiogenic) or bacterial infection (septic).
Treatment Options
To treat minor dehydration water intake must be increased, while the source of fluid loss must be reduced or stopped altogether. Plain water restores only the volume of the blood plasma and inhibits the thirst mechanism before solute levels can be replenished.
Solid foods can contribute to fluid loss from vomiting and diarrhea. In more severe cases, correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes through oral rehydration therapy or fluid replacement by intravenous therapy (an IV drip).
As oral rehydration is easier to provide, it is the treatment of choice for mild dehydration. Solutions used for intravenous rehydration must be isotonic or hypotonic. Pure water injected into the veins will cause the breakdown (lysis) of red blood cells that could cause other problems.
Amyopathic Dermatomyositis (ADM)/Dermatomyositis is a rare acquired or autoimmune humoral-mediated muscle disease characterized by muscle weakness and a skin rash that causes muscle inflammation and disease condition in which antigen-specific antibodies are deposited in the microvasculature, either secondary to immune complex deposition or specific anti-endothelial cell binding [rx, rx]. It presents with symmetric proximal muscle weakness, skin rash, and extramacular manifestations, such as esophageal dysfunction and interstitial lung disease. Dermatomyositis is strongly associated with malignancy, especially in adults. This activity outlines the evaluation and management of dermatomyositis and highlights the role of the interprofessional team in improving care for patients with this condition. [rx][rx] Dermatomyositis presents with characteristic skin findings and symmetric proximal skeletal muscle weakness. Also, it can affect other organ systems such as the pulmonary, cardiovascular, and gastrointestinal systems.[rx]
Dermatomyositis is a rare autoimmune inflammatory myositis of unknown etiology affecting both children and adults. It involves striated muscles and skin. The juvenile form is associated with multisystemic vasculitis and a high frequency of calcinosis. However, unlike the adult form, it does not have an increased risk of malignancy. This activity explains when this condition should be considered, articulates how to properly evaluate for this condition, and highlights the interprofessional team’s role in caring for patients with this condition.
Types of Dermatomyositis
There are 6 different types of DM; they are
Classic dermatomyositis (CDM),
Amyopathic dermatomyositis (ADM),
Homeopathic dermatomyositis (HDM),
Amyopathic dermatomyositis (CADM), which evolves into classic DM (CADM → CDM) and juvenile dermatomyositis (JDM).[rx]
CDM is defined as the hallmark cutaneous manifestation with signs of proximal muscle weakness after the onset of skin disease within the first 6 months.[rx]
ADM is also associated with cutaneous involvement, it may occur within 6 months or greater of DM diagnosis, without any clinical or laboratory evidence of any skin or muscle disease.[rx] In HDM, there is no subjective muscle weakness, especially after the first 6 months.
Causes of Dermatomyositis
The cause is unknown, but it may result from an initial viral infection or cancer, either of which could raise an autoimmune response.[rx]
Between 7 and 30% of dermatomyositis arises from cancer, probably as an autoimmune response.[rx] The most commonly associated cancers are ovarian cancer, breast cancer, and lung cancer.[rx] 18 to 25% of people with amyopathic DM also have cancer.[rx] Malignancy in association with dermatomyositis is more prevalent after age 60. Some cases are inherited, and HLA subtypes HLA-DR3, HLA-DR52, and HLA-DR6 seem to create a disposition to autoimmune dermatomyositis.[rx]
Although the cause of dermatomyositis is unknown, several genetic, immunologic, and environmental factors are implicated in this condition.
Genetic Factors – Multiple studies have indicated that patients with particular human leukocyte antigen (HLA) types are at higher risk of dermatomyositis. High-risk haplotypes include HLA-A68 in North American Whites[rx], HLA-DRB1*0301 in African Americans,[rx] HLA-DQA10104, and HLA-DRB107 in Han Chinese,[rx] DQA105 and DQB1*02 in people from the UK. Also, the DRB103-DQA105-DQB102 haplotype is strongly associated with the development of interstitial lung disease in dermatomyositis.[rx]
Immunologic Factors – Although autoantibodies are detected in patients with dermatomyositis, it is unclear whether they play a role in pathogenesis.
Infections – Viruses such as Coxsackie B virus, enterovirus, and parvovirus have been suspected of acting as triggers of dermatomyositis. There are multiple theories about the mechanisms of virus-induced autoimmunity. These include alteration of cellular proteins, breakdown of self-tolerance, an unmasking of previously hidden epitopes, autoantibody induced B cell activation, and molecular mimicry.[rx]
Drugs – Several drugs can trigger dermatomyositis. These include antineoplastic drugs (hydroxyurea, cyclophosphamide), anti-infectious agents (penicillin, sulfonamides, isoniazid), non-steroidal anti-inflammatory drugs (diclofenac, phenylbutazone), D-penicillamine, statins, and certain vaccines.[rx]
Radiation – Dermatomyositis has been observed to occur more frequently among women exposed to high-intensity ultraviolet radiation.[rx]
Genetic susceptibility is no longer in doubt since predisposing HLA systems have been identified. There is an activation of the complement leading to the deposition of the membrane attack complex in the wall of blood vessels, which causes microangiopathy and an inflammatory reaction.
Because the disorder appears to have seasonal clustering, it is believed that some infectious organisms may be playing a role in self-tolerance and the generation of the autoimmune response. Infections implicated include:
Parvovirus B19
Coxsackievirus
Streptococcus
Enteroviruses
Non-infectious agents implicated include silica exposure, silicone implants, and medications that decrease lipids. There is a strong association of JDM with HLA-DR3.
Symptoms of Dermatomyositis
The signs and symptoms of dermatomyositis can appear suddenly or develop gradually over time. The most common signs and symptoms include
Skin changes – A violet-colored or dusky red rash develops, most commonly on your face and eyelids and on your knuckles, elbows, knees, chest, and back. The rash, which can be itchy and painful, is often the first sign of dermatomyositis.
Muscle weakness – Progressive muscle weakness involves the muscles closest to the trunk, such as those in your hips, thighs, shoulders, upper arms, and neck. The weakness affects both the left and right sides of your body and tends to gradually worsen.
Common characteristics of DM include proximal muscle weakness, muscle inflammation, and skin rash
Skin involvement in DM usually manifests with characteristic papules over digits, erythema over the elbows and knees, a heliotrope rash around the eyes, periungual telangiectasias, and dystrophic cuticles.[rx] Muscle involvement usually manifests as proximal muscle weakness initially, with or without myalgias or tenderness. An amyopathic variant with minimal to no muscle inflammation has been described.[rx] There is a well-established association of DM with an increased risk of internal malignancy.[rx]
One form the rashes take is called “heliotrope” (a purplish color) or lilac, but may also be red. It can occur around the eyes along with swelling, but also occurs on the upper chest or back what is called the “shawl” (around the neck) or “V-sign” above the breasts and may also occur on the face, upper arms, thighs, or hands.[rx] Another form the rash takes is called Gottron’s sign which are red or violet, sometimes scaly, slightly raised papules that erupt on any of the finger joints (the metacarpophalangeal joints or the interphalangeal joints).[rx][rx] Gottron’s papules may also be found over other bony prominences including the elbows, knees, or feet. All these rashes are made worse by exposure to sunlight, and are often very itchy, painful, and may bleed.[rx]
Diagnosis of Dermatomyositis
History
The typical histopathologic findings of DM in muscle include perifascicular atrophy, endothelial cell swelling, vessel wall membrane attack complex (MAC) deposition, papillary necrosis, infarcts, major histocompatibility complex (MHC) I upregulation, and the presence of an inflammatory infiltrate consisting of T and B lymphocytes, macrophages, and plasma cells.[rx]
A comprehensive history and physical exam should be conducted in suspected cases of dermatomyositis, keeping in mind the following objectives:
Identify the typical muscular and cutaneous signs and symptoms of dermatomyositis
Exclude other causes of muscle weakness e.g., inherited, infectious or endocrine myopathy
Conduct a detailed review of systems to determine if other organ systems are involved (respiratory, cardiac, esophageal)
Evaluate for signs and symptoms of a possible underlying malignancy and perform age-appropriate cancer screening when indicated
Muscle weakness and skin findings comprise the main presenting symptoms in dermatomyositis. The onset of the disease may be insidious or acute with a waxing and a waning course.
Physical Examination
The hallmark clinical feature of IIM is symmetric proximal muscle weakness. It is manifested as difficulty in getting up from sitting position, climbing stairs, lifting heavy objects, and overhead abduction of the arm. In addition to muscle weakness, patients with dermatomyositis (DM) often present with a characteristic skin rash. Gottron papule and heliotrope rash are the pathognomonic skin finding of DM.
Description of the major skin findings in DM is given below
Heliotrope rash – Violaceous rash on the eyelids sometimes associated with periorbital edema
Gottron papules – Erythematous rash with variable papules on the extensor aspect of digits (metacarpophalangeal, proximal interphalangeal, and distal interphalangeal joints)
Gottron sign – Erythematous papules, macules, or patches on sites other than hands, particularly extensor surfaces of elbows, knees, and ankles.
Shawl sign – Erythematous rash on the anterior chest (in a V-sign) and upper back
Mechanic’s hands – Dilated capillary loops at the base of the fingernails, irregular and thickened cuticles, and cracked palmar fingertips
Holster sign – Poikiloderma on the lateral aspects of the thigh (areas protected from sunlight)
These lesions (except holster sign) are photosensitive and may be aggravated by ultraviolet radiation. Other manifestations include dystrophic cuticles, peri-ungual erythema, abnormal nail bed capillary loops, diffuse flat erythema over the forehead, chin, and knees; photosensitivity; shawl sign; V-sign; panniculitis; and calcinosis cutis.
Dermatomyositis includes several clinically distinct phenotypes, and specific autoantibodies are associated with each unique phenotype.
Muscular
Muscle weakness is the most common presenting symptom in dermatomyositis. The weakness usually has a subacute onset with the development of gradually progressive symmetric proximal muscle weakness. Patients may report difficulty in carrying out activities such as climbing stairs, getting up from a seated position, lifting objects, combing hair, and raising their head from a pillow.
Distal muscle weakness, muscle pain, and stiffness are uncommon in dermatomyositis. In severe cases, dysphagia, or dysphonia may be present. The examination may reveal reduced muscle strength of proximal muscles, such as the deltoids, hip flexors, and neck flexors. Usually, muscle tenderness is mild, and distal muscle strength is preserved. Depressed deep tendon reflexes and muscle atrophy are not seen unless the disease is severe and long-standing.
Cutaneous
Skin changes may precede or may coincide with the onset of muscular symptoms. Patients can present with several types of skin rashes, photosensitivity, changes in pigmentation, and pruritis. Dermatomyositis can also cause nail changes and alopecia.
Pathognomonic findings of dermatomyositis include the following:
Gottron papules – dorsal metacarpophalangeal and interphalangeal joints may show the presence of overlying erythematous or violaceous papules with or without scaling or ulceration.
Heliotrope rash – This is a characteristic skin finding of dermatomyositis and presents with a violaceous, or an erythematous rash affecting the upper eyelids with or without periorbital edema. This finding may not be apparent in patients with dark skin patients.
Other skin findings that may help differentiate dermatomyositis from other conditions include the following
Gottron sign – erythematous macules or patches over the elbows or knees
Facial erythema – erythema over the cheeks and nasal bridge involving the nasolabial folds. The rash may extend up to the forehead and laterally up to the ears.
Shawl sign – erythema over the posterior aspect of the neck, upper back, and shoulders at times, extending to the upper arms.
V sign – ill-defined erythematous macules involving the anterior aspect of the neck and the upper chest.
Poikiloderma – atrophic skin with changes in pigmentation and telangiectasia in photo-exposed or non-exposed areas.
Holster sign – poikiloderma involving the lateral aspects of the thighs.
Periungual involvement – telangiectasias and cuticular overgrowth
Mechanic’s hands – hyperkeratotic, cracked horizontal lines on the palmar and lateral aspects of the fingers.
Scalp involvement – diffuse poikiloderma, with scaling and pruritis.
Calcinosis cutis – calcium deposits in the skin
Associate
Joints – Dermatomyositis can cause non-erosive polyarthritis or arthralgia of the small joints of the hands. Patients may present with joint pain or swelling.
Respiratory – Patients may present with exertional dyspnea, exercise intolerance, and non-productive cough due to underlying interstitial lung disease (ILD). Auscultation of the chest may reveal the presence of bilateral dry crackles. Reduced chest movement may be seen due to respiratory muscle weakness.
Esophageal – Patients may report difficulty swallowing solids and liquids due to the weakness of the muscles of the oropharynx and upper esophagus. They may also have symptoms of gastroesophageal reflux.
Other findings – Other findings that may present in dermatomyositis include Raynaud’s phenomenon, gastrointestinal ulcers, and cardiac symptoms. Systemic symptoms such as fever, malaise, and weight loss may be present, which may indicate an occult malignancy. The following factors may predict malignancy; male gender, older age at onset, the presence of dysphagia, and the absence of interstitial lung disease.[rx].
Muscle Biopsy
Muscle biopsy often shows the following findings, which can be diagnostic
Perivascular and perimysial inflammatory infiltrate – The infiltrate in dermatomyositis is concentrated around the perivascular and interfascicular regions and consists of B cells, CD4+ T helper cells, macrophages, and plasmacytoid dendritic cells. In contrast to polymyositis, CD8+ T cells and NK cells are rarely present.
Perifascicular atrophy – Atrophy of muscle fibers, especially around the periphery of fascicles, is a hallmark histopathological feature of dermatomyositis. Degenerating and regenerating muscle fibers may be observed in the perifascicular region.
Microangiopathy – Injury to intramuscular blood vessels takes the form of immunoglobulin and complement (C5b-C9 membrane attack complex) deposits on endomysial capillaries. A reduced capillary density and endothelial hyperplasia may be observed.[rx][rx]
Skin Biopsy
Skin biopsy findings in dermatomyositis are similar to those found in systemic lupus erythematosus. Typical findings include vacuolar changes of the basal layer, increased lymphocytic infiltrate, and increased mucin deposition in the dermis.[rx]
Lab Investigations
Muscle Enzymes – Initial testing in suspected cases of dermatomyositis should include muscle enzymes, such as creatine kinase (CK), aldolase, lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Testing for muscle enzymes helps to guide further diagnostic studies and to assess response to therapy. In some cases, the elevation of muscle enzymes occurs prior to the appearance of muscle weakness.
Autoantibodies – Antinuclear antibodies (ANA) are present in a majority of patients with dermatomyositis but do not help to make a diagnosis. Instead, testing should focus on detecting myositis-specific autoantibodies (MSA), which are present in approximately 30% of dermatomyositis and polymyositis patients. Testing for myositis-specific antibodies offers valuable information for determining the prognosis and can help to predict the pattern of organ involvement. Aminoacyl-transfer (t) ribonucleic acid synthetase (also known as an antisynthetase antibody) is the most common myositis-specific autoantibody associated with dermatomyositis. Anti-Jo is the most common antisynthetase antibody found in dermatomyositis.
An abnormal elevation of serum – activities of muscle enzymes is the most common biological finding in JDM. Elevation of creatine kinase is expected in 75% to 85% of cases with average values around 2000 U/L plus or minus 1000. A normal rate can be observed at the beginning of the disease and in amyopathic forms. Regular creatine phosphokinase (CPK) monitoring is recommended during the evolution under treatment to evaluate its effectiveness.
The following autoantibodies are associated with specific complications and findings
Anti-Jo – antisynthetase syndrome consisting of interstitial lung disease, mechanic’s hands, Raynaud phenomenon, sclerodactyly, and arthritis.
Anti-NXP2 (nuclear matrix protein 2) – calcinosis cutis[rx]
Electromyography (EMG)
Electromyography helps to identify which groups of muscles are most affected and provides guidance about which muscles to biopsy. It also helps to distinguish dermatomyositis from neuropathic conditions. However, the electromyographic findings are not specific and may be absent in 11% of patients.[rx] Findings suggestive of dermatomyositis include the following:
Increased insertional activity
Spontaneous fibrillations
Positive sharp waves
Complex repetitive discharges
Early recruitment
Low-amplitude, short polyphasic motor unit potentials
Radiology
Chest radiography – Every patient with dermatomyositis should undergo chest radiography to screen for interstitial lung disease. If the patient has respiratory symptoms or abnormal chest X-ray findings, further testing with high-resolution computer tomography (HRCT) of the chest. In addition, pulmonary function tests should be performed. Findings on HRCT suggestive of interstitial lung disease include nodules, fibrosis, linear opacities, honey-combing, or consolidation.
Magnetic resonance imaging (MRI) – Magnetic resonance imaging of skeletal muscles is a non-invasive and sensitive test to evaluate myositis. Typical findings include muscle edema, areas of inflammation; that appear hyperintense on T2-weighted images; and fat suppression.[rx]
Barium swallow – may be done if esophageal dysfunction is present.
Using testing of electric signaling in muscles, finding all three of – erratic, repetitive, high-frequency signals; short, low-energy signals between skeletal muscles and motor neurons that have multiple phases; and sharp activity when a needle is inserted into the muscle
Histopathology
Muscle biopsy is the most accurate test to confirm the diagnosis of dermatomyositis and to exclude other causes of muscle weakness or skin rash. However, choosing the right muscle for a biopsy is crucial to prevent a missing diagnosis.
Muscle biopsy should be obtained on weak muscles as identified by physical exam or contralateral to the abnormal muscles, as identified by electromyography.
A muscle biopsy should be obtained from patients with suspected dermatomyositis but who lack the characteristic skin findings. Similarly, patients who have the characteristic skin manifestations of dermatomyositis but lack muscle weakness should undergo a skin biopsy procedure.[rx]
Other Investigations
Other baseline lab investigations include
Using a blood test, finding higher levels of enzymes found in skeletal muscle, including creatinine kinase, aldolase, and glutamate oxaloacetate, pyruvate transaminases and lactate dehydrogenase
A complete blood count with differential,
Creatinine,
Liver function tests, and inflammatory markers
Erythrocyte sedimentation rate (ESR) and
C-reactive protein (CRP)
Serum Thyroid-stimulating hormone (TSH) may be ordered to exclude hypothyroidism.
Electrocardiography (ECG) may be ordered to look for conduction abnormalities that might be subclinical.
Pulmonary function tests may be conducted to assess the severity of pulmonary involvement. Patients with interstitial lung disease show a restrictive defect on pulmonary function tests with reduced forced vital capacity (FVC), reduced total lung capacity (TLC), and diminished diffusing capacity.
Investigations for Malignancy
Colonoscopy (or fecal occult blood test),
Urine analysis, mammography, and pap smears. Women at high risk of ovarian cancer should be screened, with serial measurements of CA-125 and
Transvaginal ultrasound. There is no consensus on the frequency and how extensively patients with dermatomyositis should undergo cancer screening. [rx]
Treatment of Dermatomyositis
The goals of managing dermatomyositis are focused on treating muscle weakness, skin disease, and addressing any other underlying complications.
Medications
Medications used to treat dermatomyositis include:
Systemic glucocorticoids – The first-line treatment of muscle disease in dermatomyositis is systemic glucocorticoids with or without immunosuppressants. Although there is no standard systemic steroid regimen specified for dermatomyositis, the general principles of therapy are the same. Although systemic glucocorticoids can control muscle disease, they are not effective in controlling skin disease.
Prednisolone – is given at high doses for the first few months until the muscle enzyme levels decline, and muscle strength improves. During this time, patients should be regularly evaluated for an adequate response, keeping in mind that it takes approximately six weeks for muscle enzymes to normalize. Also, it may require as long as three months for muscle weakness to improve. Once an adequate response occurs, the administration of systemic steroids is gradually tapered off over time. The total duration of therapy with systemic steroids usually spans between nine and twelve months. It is important to note that administering high-dose glucocorticoids for more than six weeks may lead to glucocorticoid myopathy.
Immuno-suppressants – First-line agents include azathioprine and methotrexate. Administration of an immuno-suppressant such as azathioprine is preferred in patients with liver involvement, interstitial lung disease, and those who are unable to abstain from alcohol. On the other hand, methotrexate has the advantage of once-a-week dosing. The choice of immunosuppressant depends on many factors, including dosing frequency, systemic involvement, adverse effects, and alcohol use. Patients who do not respond satisfactorily to therapy with steroids and azathioprine or methotrexate are considered resistant. Treatment options for resistant cases include rituximab, mycophenolate mofetil, calcineurin inhibitors, intravenous immunoglobulin (IVIG), and cyclophosphamide. Rituximab is an anti-CD 20 agent and is the recommended first-line agent in resistant cases. If this fails, intravenous immunoglobulin or a combination of azathioprine and methotrexate can be used as second-line therapy. Mycophenolate mofetil and tacrolimus are useful in refractory cases, especially if there is a concomitant interstitial lung disease. Cyclophosphamide is preferred in cases of rapidly progressive interstitial lung disease.
Cotreatment with folic acid or leucovorin – can help to minimize these adverse effects. Azathioprine can cause a flu-like reaction, which may require discontinuation of therapy. It also causes myelosuppression and pancreatitis. Cyclophosphamide increases the risk of malignancy and should be avoided unless multiple drug therapies have failed.
Corticosteroid-sparing agents – When used with a corticosteroid, these drugs can decrease the dose and side effects of the corticosteroid. The two most common medications for dermatomyositis are azathioprine (Azasan, Imuran) and methotrexate (Trexall). Mycophenolate mofetil (Cellcept) is another medication used to treat dermatomyositis, particularly if the lungs are involved.
Antimalarial medications – For a persistent rash, your doctor might prescribe an antimalarial medication, such as hydroxychloroquine (Plaquenil).
Sunscreens – Protecting your skin from sun exposure by applying sunscreen and wearing protective clothing and hats is important for managing the rash of dermatomyositis. These measures should include sun-protective measures, such as sunlight avoidance, the use of sun-protective clothing, and sunscreen with sun protective factor (SPF) of 30 or higher.
Cream, patches, gel, ointment – due to skin disease can be disabling and can be managed by employing local agents (pramoxine, menthol, camphor) or oral drugs (e.g., sedating antihistamines, amitriptyline, gabapentin). Medical therapy for skin disease includes topical agents and systemic medications. Topical agents include corticosteroids and calcineurin inhibitors. The most commonly used systemic agents to treat skin disease are hydroxychloroquine and methotrexate.
Calcinosis – which occurs more frequently in juvenile dermatomyositis, can be managed with calcium channel blockers such as diltiazem. In some cases, surgical removal of calcinotic nodules may be indicated. Adjunctive hygienic-dietary measures, as well as daily supplementation with calcium and vitamin D, must be systematic.
Vitamin E capsule – Vitamin E is a group of eight fat-soluble compounds that include four tocopherols and four tocotrienols. Vitamin E deficiency, which is rare and usually due to an underlying problem with digesting dietary fat rather than from a diet low in vitamin E, can cause nerve problems.
Vitamin B Complex – is a class of water-soluble vitamins that play important roles in cell metabolism. Though these vitamins share similar names, they are chemically distinct compounds that often coexist in the same foods. In general, dietary supplements containing all eight are referred to as a vitamin B complex. Individual B vitamin supplements are referred to by the specific number or name of each vitamin.
Anti-resorptive therapy – may be indicated in patients on long-term systemic corticosteroids in order to prevent osteoporosis. Patients on high-dose systemic glucocorticoids or immunosuppressants should be considered for prophylaxis against Pneumocystis jiroveciiwith trimethoprim and sulfamethoxazole. Lastly, all patients should receive the appropriate immunizations prior to receiving immunosuppressants.
Therapy
Physical therapy and rehabilitation play an essential role in management. Patients with mild disease should be encouraged to participate in active exercise programs. Range of motion exercises can help in preventing contractures. Patients with esophageal dysfunction may require consultation with speech therapy and may also require measures to prevent aspiration. Anti-aspiration measures include elevation of the head off the bed, thickening of feeds, and even feeding via gastric tubes when indicated.
Depending on the severity of your symptoms, your doctor might suggest
Physical therapy – A physical therapist can show you exercises to help maintain and improve your strength and flexibility and advise you about an appropriate level of activity.
Speech therapy – If your swallowing muscles are affected, speech therapy can help you learn how to compensate for those changes.
Dietetic assessment – Later in the course of dermatomyositis, chewing and swallowing can become more difficult. A registered dietitian can teach you how to prepare easy-to-eat foods.
Surgical and other procedures
Intravenous immunoglobulin (IVIg) – IVIg is a purified blood product that contains healthy antibodies from thousands of blood donors. These antibodies can block the damaging antibodies that attack muscle and skin in dermatomyositis. Given as an infusion through a vein, IVIg treatments are expensive and might need to be repeated regularly for the effects to continue.
Surgery – Surgery might be an option to remove painful calcium deposits and prevent recurrent skin infections.
Casino is a facility for certain types of gambling. Casinos are often built near or combined with hotels, restaurants, retail shopping, cruise ships, and other tourist attractions. Some casinos are also known for hosting live entertainment, such as stand-up comedy, concerts, and sports.
Etymology and usage
The casino is of Italian origin; the root casa means a house. The term casino may mean a small country villa, summerhouse, or social club.[rx] During the 19th century, the term casino came to include other public buildings where pleasurable activities took place; such edifices were usually built on the grounds of a larger Italian villa or palazzo and were used to host civic town functions, including dancing, gambling, music listening, and sports. Examples in Italy include Villa Farnese and Villa Giulia and in the US the Newport Casino in Newport, Rhode Island. In modern-day Italian a casino is a brothel (also called casa chiusa, literally closed house), a mess, or a noisy environment; a gaming house is spelled casinò, with an accent.[rx][rx][rx]
Not all casinos are used for gaming. The Catalina Casino, overlooking Avalon Harbor on Santa Catalina Island, California, has never been used for traditional games of chance, which were already outlawed in California by the time it was built.,[rx] The Copenhagen Casino was a theatre, known for the mass public meetings often held in its hall during the 1848 Revolution, which made Denmark a constitutional monarchy. Until 1937, it was a well-known Danish theatre.[rx] The Hanko Casino in Hanko, Finland—one of that town’s most conspicuous landmarks—was never used for gambling. Rather, it was a banquet hall for the Russian nobility which frequented this spa resort in the late 19th century and is now used as a restaurant.[rx] . In military and non-military usage in German and Spanish, a casino or kasino is an officers’ mess.
History of gambling houses
The precise origin of gambling is unknown. It is generally believed that gambling in some form or another has been seen in almost every society in history. From the Ancient Greeks and Romans to Napoleon’s France and Elizabethan England, much of history is filled with stories of entertainment based on games of chance.
The first known European gambling house, not called a casino although meeting the modern definition, was the Ridotto, established in Venice, Italy, in 1638 by the Great Council of Venice to provide controlled gambling during the carnival season. It was closed in 1774 as the city government felt it was impoverishing the local gentry.[rx]
In American history, early gambling establishments were known as saloons. The creation and importance of saloons were greatly influenced by four major cities: New Orleans, St. Louis, Chicago, and San Francisco. It was in the saloons that travelers could find people to talk to, drink with, and often gamble with. During the early 20th century in America, gambling was outlawed by state legislation. However, in 1931, gambling was legalized throughout the state of Nevada, where America’s first legalized casinos were set up. In 1976 New Jersey allowed gambling in Atlantic City, now America’s second largest gambling city.
Gambling in casinos
Slot machines in Atlantic City. Slot machines are a standard attraction of casinos
Customers gamble by playing games of chance, in some cases with an element of skill, such as craps, roulette, baccarat, blackjack, and video poker. Most games have mathematically determined odds that ensure the house has at all times an advantage over the players. This can be expressed more precisely by the notion of expected value, which is uniformly negative (from the player’s perspective). This advantage is called the house edge. In games such as poker where players play against each other, the house takes a commission called the rake. Casinos sometimes give out complimentary items or comps to gamblers. Payout is the percentage of funds (“winnings”) returned to players. Casinos in the United States say that a player staking money won from the casino is playing with the house’s money.
Video Lottery Machines (slot machines) have become one of the most popular forms of gambling in casinos. As of 2011 investigative reports have started calling into question whether the modern-day slot-machine is addictive.[rx]
What Is The Most Natural Sleep Position/ Generally, the best sleeping position for you is the one that allows you to have the most REM sleep (that magical “deep sleep” when you dream and when your eyes dart from side-to-side). All parts of the sleep cycle are important, but REM sleep is the most restorative and vital for memory retention. Without enough of it throughout the night, you can wake up with a headache and achy feeling all over. Seriously, the long-term effects of sleep deprivation and consistent low-quality sleep are just scary
Wondering which sleep spot is best? Check out the rankings, below, from best to worst.
Back Care for Sleeping Position
Though it’s not the most popular position—only eight percent of people sleep on their backs—it’s still the best. By far the healthiest option for most people, sleeping on your back allows your head, neck, and spine to rest in a neutral position. This means that there’s no extra pressure on those areas, so you’re less likely to experience pain. Sleeping facing the ceiling also ideal for warding off acid reflux. Just be sure to use a pillow that elevates and supports your head enough—you want your stomach to be below your esophagus to prevent food or acid from coming up your digestive tract. However, snoozing on your back can cause the tongue to block the breathing tube, making it a dangerous position for those who suffer from sleep apnea (a condition that causes periods of breathlessness). This position can also make snoring more severe.
Side Sleepers
Side sleepers are numerous (making up a whopping 63 percent of all sleepers). We’re a versatile bunch, with all kinds of subsets including the log, the yearner, and the fetal position (more on that last one below).
Side Sleeping Benefits
Sleeping on your side is great for cuddling and pillow-talk. Additionally, research suggests that sleeping on your left side is preferable to your right. Thanks to the unique arrangement of your internal organs, left-side sleepers may see benefits in improved digestion and blood flow. It can also help reduce heartburn.
Side Sleeping Cons
One of the biggest drawbacks to sleeping on your side is the dreaded numb arm. Also, it can lead to shoulder pain, hip pain, and back pain if your spine, neck, and hips aren’t properly aligned throughout the night. It also puts more strain on your pressure points. All of these symptoms can be lessened with the help of a quality mattress and various arrangements of pillows to suit your personal style.
Side sleeping can lead to more face wrinkles (because you’re pressing your face against the pillow all night) and saggy breasts (because of …gravity).
How to Sleep on Your Side Like a Pro
The side sleeper secret is to keep your back as straight as possible. The best way to achieve this, big surprise, is with a great mattress. Find a mattress that provides support for the curvature of your body while still embracing the pressure points of your shoulders and hips.
Other helpful side-sleeping techniques are to position a pillow between your legs and use a tall pillow that aligns your neck better with your back (as opposed to sleeping with your head cocked to one side like you can’t understand what I’m saying but you’re going to pretend as you do anyway).
Fetal Position Sleepers
The fetal position is the close, adorable cousin to the side sleeper. While some of us only curl up in a fetal position when we’d rather not be adults for a while, a whopping 41 percent of people prefer this style of sleep position.
Fetal Position Sleeping Benefits
The most obvious benefit of sleeping in a fetal position is that it makes you a great little spoon. There’s also evidence that fetal-sleepers are shy and sensitive, but with a hard shell on the outside that can be tough to crack, but totally worth it. We get it, fetal-position sleepers, you’re super cute. Beyond that, you get all the benefits of the side sleeper, as well. It’s an all-around solid sleep choice!
Fetal Position Sleeping Cons
Being too curled up in the fetal position can cause your lower back to arch in an unnatural manner, leading to aches and pains in the morning.
How to Make the Most of the Fetal Position
Try to bring those legs down a touch so that your body is straighter. And put a small pillow between your legs to relieve some pressure on your spine so you can cuddle the night away.
Back Sleepers
If you’re a back sleeper, take some pleasure in knowing that sleeping on your back is often recommended as the best position for preventing aches and pains in the morning.
Back Sleeping Benefits
Sleeping on your back gives you your best shot at resting your spine in its most natural position. In fact, your entire skeleton will thank you for sleeping on your back, because your arms, shoulders, and legs won’t be jammed under the weight of your body or contorted in some bizarre amusement-park-ride pose.
Back Sleeping Cons
Unfortunately, back sleepers don’t have it all good. It can lead to problems with snoring since gravity pulls your tongue to the back of your throat, and it isn’t recommended for people who suffer from sleep apnea.
In young adults, scientists have noted that poor sleepers typically spend more time on their backs than other positions, so sleeping on your back doesn’t necessarily mean you’ll get the best night’s rest of your life.
How to Make the Most of Sleeping on Your Back
If snoring is a problem, either find another position (or another sleep partner) OR rock some snoring aids like nasal strips and mouthpieces. And don’t forget to find that ideal mattress that provides the best spinal alignment.
Stomach Sleepers
If you’re one of 7 percent of the population who sleep on their stomach, you’re a special breed. More often, you’re brash and gregarious. You also don’t like criticism, so we’re not going to chastise you for sleeping in the least-recommended position.
Stomach Sleeping Benefits
Stomach-sleeping can reduce snoring and help in some cases of sleep apnea. Unfortunately, there isn’t much of a benefit beyond that.
Stomach Sleeping Cons
If you’re a stomach sleeper, we love you, but your sleep style probably isn’t doing you any favors. Having your head jammed to the side all night can lead to a sore neck in the morning. Lying chest-down straightens your spine into an unnatural position, leading to all kinds of lower back pain. And if you’re pregnant? Fuhgeddaboudit.
How to Make the Most of Stomach Sleeping
If sleeping on your stomach really is the best way you can get a quality night’s rest, then here are a few ways to make it more comfortable:
Switch out that thick pillow for a razor-thin one (or no pillow at all)
Prop a pillow under your pelvis to add some curve to your spine
Do some stretches in the morning to ease back pain
Best Sleep Positions for Couples
Adding another person into the mix can definitely throw your sleep position game off, but it doesn’t have to. In fact, 94 percent of couples who cuddle (or at least have some kind of physical contact) through the night report being happy with their relationship. Meanwhile, only 68 percent of couples who don’t touch through the night report relationship satisfaction. So, while there are plenty of variations of the above sleeping positions for couples, the best position for you and your partner is the one where:
You both get the best, high-quality rest
You touch in some way (unless that interferes with the above point)
A child or pet isn’t kicking you all night and commandeering the entire mattress
Also, a king size bed is the largest and best bed for couples, then you can sleep in any position you want.
The Best Sleep Position for Pregnant Women
If you’ve got a bundle of joy cradled inside your abdomen, it can make finding a comfortable sleeping position just a tad challenging. Also, you want to be sure that you’re not doing anything that could cause problems with your pregnancy or harm your baby in any way.
So what’s the best sleep position for pregnant women? As it turns out, sleeping on your left side is the best. It improves blood circulation and doesn’t put pressure on your liver. It’s even better to have your legs bent (again, to aid in good blood circulation) with a small pillow between your knees.
If you find it difficult to sleep on your left side during pregnancy (after all, many aspects of pregnancy are going to be uncomfortable, what with a sentient being growing inside you and all) try propping up various parts of your body with pillows. Pillows are your best friend. Stack ‘em up all around you until you find the comfort you so desire.
Tips for Transitioning to a New Sleep Position
The inevitable transition period required to get used to a new sleep position can be difficult. That’s in large part because you’ll likely be getting some pretty lousy sleep while your body gets used to your new position.
But, if you’re determined to change the way you sleep, here are some tips to shorten the transition period and start your new life of sleeping bliss!
Block out all natural light in your room and banish electronic devices from your life for the two hours leading up to your bedtime.
Sleep on the opposite side of your bed from what you usually do. Your body may be less likely to revert automatically to your old position.
Don’t skimp on extras like a high-quality pillow and stretchy mattress covers and sheets.
You might have to be persistent for a while if you truly want to make a change to your sleeping habits. But if your goal is to reduce back pain and ultimately improve the quality of your sleep, it may be well worth it.
Sleeping Bad Habit That Must be Change
Don’t go to bed with cold feet – Warm your feet every time before going to bed
Not having a bedtime routine – Set up a routine before going to bed to teach your brain when is time to sleep, like brushing your teeth, washing your face, etc.
Avoid drinking coffee 4 hours before going to bed – Caffeine is very bad and keep you awake for a longer time.
Avoid certain sleeping positions – Experts advise sleeping on the left side as a better position for your body to rest.
Keep the electronic devices away from the bed – Scrolling on your phone or tablet before going to bed can have a very negative effect because the brightness from the screen prevents the brain from falling asleep.
Believe it or not, you should avoid books as well – Reading before bedtime is also known as a way to keep you awake for a longer period of time.
Avoid a bright alarm clock – Light or anything similar can drag your attention and disturb your sleep and you will not wake up rested in the morning.
Don’t drink any fluids an hour before going to bed – Fluids make you go to the bathroom more often and it will disturb your sleep.
Avoid afternoon naps – Afternoon naps make you feel rested longer and your body doesn’t need sleep. It also changes your sleeping routine so try to avoid them.
Don’t sleep on a low-quality mattress – Quality mattresses are very important for a night of good night sleep. You will wake up rested and energized.
Don’t eat 2 hours before going to bed – When you lie down with a full stomach, you won’t fall asleep fast as the digestion process keeps the body awake.
Avoid exercising 3 hours before going to bed – When you exercise your body fills with adrenaline and this is the reason you can’t go to sleep quickly.
Confusion Diagnosis/Confusion is a common neuropsychiatric syndrome in the elderly. The DSM-IV-TR defines delirium as a “disturbance of consciousness and a change in cognition that develop ois a common neuropsychiatric syndrome in the elderly. The DSM-IV-TR defines delirium as a “disturbance of consciousness and a change in cognition that develop over a short period of time. The syndrome includes fluctuations in consciousness over the course of the day, a reduced ability to focus, sustain and shift attention, and evidence that the disturbance is caused by the direct physiological consequence of a medical condition [rx].
In general, the prevalence of delirium is dependent on several factors, including the patient population, care setting, the method of study and diversity of antecedent events. The prevalence of delirium in the community is 1–2%, but increases in the setting of general hospital admissions to 6–56% [rx], with the higher prevalence associated with increased age [rx] and increased severity of medical illness [rx].
Pathophysiology
Alcohol acts as central nervous system depressant. It enhances the effect of inhibitory neurotransmitters while down-regulating excitatory neurotransmitters. Alcohol interacts with GABA receptors, chloride ion receptor acting as an inhibitory neurotransmitter, via several mechanisms to enhance its activity. Over time, through prolonged alcohol exposure, there is a decrease in GABA activity and alteration in the type of GABA receptor and function. Abrupt cessation of alcohol causes a decrease in the inhibitory actions of GABA neurotransmitter resulting in overactivity of the central nervous system.
Alcohol also inhibits the action of NMDA receptor by acting as a receptor antagonist. It inhibits the action of glutamate, which is an excitatory amino acid. Prolonged alcohol abuse results in receptor up-regulation. Abrupt discontinuation of alcohol causes an increase in the action of glutamate, resulting in profound excitatory action. This may have a clinical manifestation of sympathetic overdrive, such as agitation, tremors, tachycardia, and hypertension.
Certain individuals are more vulnerable to suffer from withdrawal symptoms than others. Though the etiology remains unclear, there is a correlation between the duration of alcohol exposure and withdrawal symptoms.[rx][rx]
Types of Confusion
There are three types of delirium
Hypoactive – meaning that the person acts sleepy or withdrawn
Hyperactive – meaning that a person is agitated
Mixed – meaning that a person alternates between these two types
Delirium subtypes have been defined based on the presence (hyperactive) or absence (hypoactive) of psychomotor agitation, perceptual disturbances, and/or changes in level of consciousness.[rx] Often both subtypes are present concurrently (mixed).[rx–rx]
Causes of Confusion
Mental confusion can result from chronic organic brain pathologies, such as dementia, as well.
Neuroinflammation – Patients who develop delirium have shown an elevated PCR and Cortisol, although IL-8 is prevalent among patients in and out of ICU. The cytokines activate the endothelium and the coagulation cascade, which predisposes to microvascular thrombosis and blood flow dysfunction. The neuroinflammation leads to infiltrate cytokines and leukocytes to the hematoencephalic barrier and then in the central nervous system in which produce ischemia and neuronal apoptosis.
Cholinergic Deficiency Hypothesis – Acetylcholine is a very important neurotransmitter in attention and consciousness. It is known, acetylcholine acts as a modulator in sensory and cognitive input so, an impairment in the route leads to develop symptoms of hypoactive or hyperactive delirium, including inattention, disorganized thinking, and perceptual disturbances. Cholinergic pathways project from basal forebrain and pontomesencephalon to interneurons in the striatum and finally targets throughout the cortex.
Neurotransmitter Imbalance – The dopamine excess contributes to hyperactive delirium and is related to decreased acetylcholine. The dopaminergic and cholinergic pathways overlap in the brain, this explains why dopamine receptors impact acetylcholine levels and explain the clinical manifestations of delirium, including hyperactive and hypoactive forms. The imbalance between neurotransmitter and cholinergic pathway may result in delirium.
Chronic Stress – Activates the sympathetic nervous system and de hypothalamus-hypophysis-suprarenal glands axis, which elevate the cytokines levels and results in chronic hypercortisolism that can cause an alteration in the hippocampus function. Cortisol is the main hormone in response to stress and has deleterious effects among 5HT 1A receptors. The association between this receptors and delirium is not conclusive. High cortisol levels produce a reduction in GABA release and impairment in neuronal energy bombs.
Medications (for example, sedative hypnotics, narcotics, anticholinergic drugs, corticosteroids, polypharmacy, withdrawal of alcohol or other drugs)
Acute neurological diseases (for example, acute stroke [usually right parietal], intracranial hemorrhage, meningitis, enkephalitis)
Intercurrent illness (for example, infections, iatrogenic complications, severe acute illness, anemia, dehydration, poor nutritional status, fracture or trauma, HIV infection)
Metabolic derangement
Surgery
Environment (for example, admission to an intensive care unit)
Pain
Emotional distress
Sustained sleep deprivation
Nonmodifiable risk factors
Dementia or cognitive impairment
Advancing age (>65 years)
History of delirium, stroke, neurological disease, falls or gait disorder
Multiple comorbidities
Male sex
Chronic renal or hepatic disease
Predisposing Factors
The most important predisposing factors are listed below:[rx]
Functional dependence (e.g., requiring assistance for self-care or mobility)
Dehydration/malnutrition
Drugs and drug-dependence
Alcohol dependence
Precipitating Factors
Acute confusional state caused by alcohol withdrawal, also known as delirium tremens. Any acute factors that affect neurotransmitter, neuroendocrine, or neuroinflammatory pathways can precipitate an episode of delirium in a vulnerable brain.[rx] Clinical environments can also precipitate delirium.[rx] Some of the most common precipitating factors are listed below
Severe drop in blood pressure, relative to the patient’s normal blood pressure (orthostatic hypotension) resulting in inadequate blood flow to the brain (cerebral hypoperfusion)
Stroke/transient ischemic attack
Intracranial bleeding
Meningitis, encephalitis
Concurrent Illness
Infections – especially respiratory (e.g. pneumonia) and urinary tract infections
In surgery of cardiac, orthopedic, prolonged cardiopulmonary bypass, thoracic surgeries
Symptoms of Confusion
Inattention – As a required symptom to diagnose delirium, this is characterized by distractibility and an inability to shift and/or sustain attention.[rx]
Memory impairment – Memory impairment is linked to inattention, especially reduced formation of new long-term memory where higher degrees of attention is more necessary than for short-term memory. Since older memories are retained without need of concentration, previously formed long-term memories (i.e. those formed before the onset of delirium) are usually preserved in all but the most severe cases of delirium.
Disorientation – As another symptom of confusion, and usually a more severe one, this describes the loss of awareness of the surroundings, environment and context in which the person exists. One may be disoriented to time, place, or self.
Disorganized thinking – Disorganized thinking is usually noticed with speech that makes limited sense with apparent irrelevancies, and can involve poverty of speech, loose associations, perseveration, tangentiality, and other signs of a formal thought disorder.
Language disturbances – Anomic aphasia, paraphasia, impaired comprehension, agraphia, and word-finding difficulties all involve impairment of linguistic information processing.
Sleep changes – Sleep disturbances in delirium reflect disturbed circadian rhythm regulation, typically involving fragmented sleep or even sleep-wake cycle reversal (i.e. active at night, sleeping during the day) and often preceding the onset of a delirium episode
Psychotic symptoms – Symptoms of psychosis include suspiciousness, overvalued ideation and frank delusions. Delusions are typically poorly formed and less stereotyped than in schizophrenia or Alzheimer’s disease. They usually relate to persecutory themes of impending danger or threat in the immediate environment (e.g. being poisoned by nurses).
Mood lability – Distortions to perceived or communicated emotional states as well as fluctuating emotional states can manifest in a delirious person (e.g. rapid changes between terror, sadness and joking).[rx]
Motor activity changes: Delirium has been commonly classified into psychomotor subtypes of hypoactive, hyperactive, and mixed,[rx] though studies are inconsistent as to the prevalence of these subtypes.[rx] Hypoactive cases are prone to non-detection or misdiagnosis as depression.
Hyperactive symptoms include hyper-vigilance, restlessness, fast or loud speech, irritability, combativeness, impatience, swearing, singing, laughing, uncooperativeness, euphoria, anger, wandering, easy startling, fast motor responses, distractibility, tangentiality, nightmares, and persistent thoughts (hyperactive sub-typing is defined with at least three of the above).[rx]
Hypoactive symptoms include unawareness, decreased alertness, sparse or slow speech, lethargy, slowed movements, staring, and apathy (hypoactive sub-typing is defined with at least four of the above).[rx]
Having trouble solving problems or doing tasks that used to be easy for you.
Not knowing where you are or not recognizing family members or familiar items.
Firmly held but false beliefs (delusions).
Seeing, hearing, feeling, smelling, or tasting things that are not really there (hallucinations or illusions).
Unfounded suspicions that others are after you or want to harm you (paranoia).
Diagnosis of Confusion
Another symptom of confusion is an immense difficulty attempting to solve problems or accomplish tasks that were previously easy to perform. People suffering from confusion will also find it hard to recognize members of their own family, and even familiar objects.
Physical Examination
Examination, particularly in patients who are not fully cooperative, should focus on the following
Vital signs
Hydration status
Potential foci for infection
Skin and head and neck
Neurologic examination
Findings can suggest a cause, as with the following
Fever, meningismus, or Kernig and Brudzinski signs suggest CNS infection.
Tremor and myoclonus suggest uremia, liver failure, drug intoxication, or certain electrolyte disorders (eg, hypocalcemia, hypomagnesemia).
Ophthalmoplegia and ataxia suggest Wernicke-Korsakoff syndrome.
Focal neurologic abnormalities (eg, cranial nerve palsies, motor or sensory deficits) or papilledema suggests a structural CNS disorder.
Scalp or facial lacerations, bruising, swelling, and other signs of head trauma suggest traumatic brain injury.
DSM IV-TR Criteria for Delirium
A – Disturbance in consciousness with reduced ability to focus, sustain or shift attention.
B – A change in cognition or the development of a perceptual disturbance that is not better accounted for by a preexisting, established or evolving dementia.
C – The disturbance develops over a short period of time and tends to fluctuate over the course of the day.
D – There is evidence from history, physical examination, or laboratory findings that the disturbance is caused by the direct physiological consequences of a general medical condition.
CLINICAL SUBTYPES:
HYPERACTIVE – agitation, restlessness, with hallucinations and /or delusions
HYPOACTIVE – lethargic, difficult to arouse, minimal speech, psychomotor retardation
MIXED – symptoms of both hyperactive and hypoactive delirium
The Confusion Assessment Method (CAM) Diagnostic Algorithm.
General diagnostic criteria
(A) Disturbance of consciousness (that is, reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention
(B) A change in cognition (such as memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance that is not better accounted for by a pre-existing, established, or evolving dementia
(C) The disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day
For delirium due to a general medical condition
(D) Evidence from the history, physical examination, or laboratory findings indicates that the disturbance is caused by the direct physiological consequences of a general medical condition
For substance intoxication delirium
(D) Evidence from the history, physical examination, or laboratory findings indicates that of either (1) the symptoms in Criteria A and B developed during substance intoxication, or (2) medication use is etiologically related to the disturbance
For substance withdrawal delirium
(D) History, physical examination, or laboratory findings indicate that the symptoms in Criteria A and B developed during, or shortly after, a withdrawal syndrome
For delirium due to multiple etiologies
(D) History, physical examination, or laboratory findings indicate that the delirium has more than one etiology (for example, more than one etiological general medical condition, a general medical condition plus substance intoxication or medication side effect)
Tools for the assessment of delirium
Tool
Description
Reference
CAM
Most widely used screening test for the presence of delirium; a four-item instrument based on
DSM-III-R delirium criteria, requires the presence of acute onset and fluctuating course,
inattention, and disorganized thinking or loss of consciousness
Delirium is diagnosed when patients demonstrate an acute change in mental status or fluctuating
changes in mental status, inattention measured with either an auditory or a visual test, and either
disorganized thinking or an altered level of consciousness. Importantly, the CAM–ICU can only be
administered if the patient is arousable in response to a voice without the need for physical
stimulation
16-item scale, including 13 severity items and 3 diagnostic items. Severity scores range from 0 to
39, with higher scores indicating more-severe delirium; delirium typically involves scores ≥15
points
A structured interview detects the presence or absence of seven DSM-III criteria for delirium;
delirium is said to be present if disorientation, perceptual disturbance or disturbance of
consciousness have presented within the past 24h
Nine scaled items divided into three subscales: subscale I, information processing (score range
0–14 points), evaluates components of cognitive status; subscale II, behavior (score range 0–10
points), evaluates observed behavior and performance ability; subscale III, performance (score
range 0–16 points), assesses vital function (that is, vital signs, oxygen saturation level and urinary
incontinence). Total scores can range from 0 (minimal function) to 30 (normal function). Delirium
is present if the score is ≤ 24 points
Bedside screening tool for delirium in the intensive care unit setting; eight-item checklist based on
DSM-IV® criteria, items scored as 1 (present) or 0 (absent); a score ≥ 4 points indicates delirium
Can be used with patients unable to speak or write; assesses orientation, attention, memory,
comprehension and vigilance, primarily with visual and auditory modalities. Each individual domain
is scored 0–6 in two-point increments, except for comprehension, which is scored in single-point
increments. Total scores range from 0 to 30, with higher scores indicating better cognitive function
Abbreviations: CAM, Confusion Assessment Method; CAM–ICU, Confusion Assessment Method–Intensive Care Unit; Drs-r98, Delirium Rating Scale; DSI, Delirium Symptom Interview; DSM, Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, Arlington, VA); ICDSC, Intensive Care Delirium Screening Checklist; MDAS, Memorial Delirium Assessment Scale.
Laboratory testing – Blood and/or urine tests may be performed to determine the cause of the person’s delirium. Delirium may be the first manifestation of a severe infection or sepsis, so additional tests to identify infection may be done. A chest x-ray is often required to exclude pneumonia.
Brain imaging tests – If the cause of a person’s delirium cannot be determined based upon the history, physical examination, and laboratory testing, a computed tomography (CT) scan or magnetic resonance imaging (MRI) scan of the head may be recommended. This test can help to determine if an abnormal growth, bleeding, infection, or inflammation is present in the brain.
Lumbar puncture – During a lumbar puncture, or spinal tap, a clinician uses a needle to remove a sample of spinal fluid from the area around the spinal cord in the low back. Several tests are done on the fluid to determine if an infection (such as meningitis or encephalitis) could be causing delirium, and if so, which antibiotic treatment is best. Lumbar puncture is not recommended for every person with delirium. It may be performed if other tests are unable to determine the cause, or if there are other signs of central nervous system infection.
EEG testing – Electroencephalography (EEG) measures the electrical activity in the brain. It may be performed in a person with delirium to search for abnormal electrical activity that is commonly associated with seizures and epilepsy. It is not recommended for all people with delirium, but it may be performed if other tests are unable to determine the cause.
Differential Diagnosis
The differential diagnosis for DT includes the following
Sepsis
Uremia
Stroke
Meningitis
Encephalitis
Wernicke encephalopathy
Neuroleptic malignant syndrome
Pheochromocytoma
Drug toxicity such as with amphetamine, hallucinogen, cocaine, heroin, and PCP
Electrolyte abnormalities such as hypocalcemia and hypomagnesemia
Thyrotoxicosis
Cerebral hemorrhage
Cerebral embolism
Toxic ingestion or exposures (ethylene glycol)
Acute liver failure
Diabetic ketoacidosis
Brain abscess
Hypoglycemia
Treatment of Confusion
Any confusion that follows a trauma to the head, or immediately succeeding unconsciousness is a cause for serious concern. Even if the symptoms of confusion appear gradually over time, a person should consult a specialist for appropriate diagnosis and treatment.
There is no specific treatment for delirium. Instead, treatment focuses on several basic principles:
Avoid factors known to cause or aggravate delirium, such as certain medications
Identify and treat the underlying illness
Provide supportive and restorative care
Control dangerous and disruptive behaviors to avoid harm to the patient or others
In people with a first episode of delirium, the initial treatment is often provided in a hospital setting. This allows the health care provider to monitor the patient, begin treatment of the underlying problem, and develop a long-term care plan with the patient and/or family.
Supportive care –The goal of supportive care is to maintain the patient’s health, prevent additional complications, and avoid those factors that can aggravate delirium. This includes:
Making sure – the person gets enough to eat and drink (or providing nutrition through an IV, if needed)
Treating pain and avoiding discomfort – including avoiding constipation
Minimizing the use of restraints and bladder catheters – which can be uncomfortable, particularly to confused patients
Encouraging movement – (getting out of bed in order to walk) with necessary assistance to avoid falls
Having someone – help during meals and having the person sit upright to minimize the risk of inhaling food, drinks, and or saliva, which can lead to pneumonia
Maintaining – a regular night-day/sleep-wake cycle when possible and avoiding sleep deprivation, and maintaining a reassuring and familiar environment with one or two visiting family members or familiar objects pictures from home
Avoiding overstimulation – (eg, multiple visitors, loud noise), which can worsen delirium, but also avoiding understimulation (darkened room, complete silence)
Making hearing – aids and eyeglasses available at the hospital if the patient uses these at home
Managing behaviors – Some people with delirium have disruptive behaviors, potentially causing them to harm themselves or others. The person may say or do things that are obscene or offensive, but such behaviors do not reflect the person’s true beliefs. The person may also be at risk for falling, wandering off, or inadvertently removing intravenous lines.
Sitter – Allowing a family member or other caregiver to stay with the patient at the bedside may help to manage the patient’s behavior. This person can provide reassurance, answer questions, reorient the patient, and notify staff if the person needs assistance. In some cases, the hospital is able to provide a sitter if a family member is unavailable. However, a familiar and trusted family member or friend can provide additional reassurance to the patient.
Restraints – The use of restraints (to tie a person to their bed or chair) is almost never appropriate, as restraints can increase agitation and create additional problems by preventing the person from moving around as needed. Preventing movement also potentially allows skin sores (called pressure ulcers) to develop from sitting or lying in the same position for long periods. The use of restraints has not been shown to prevent harmful falls among hospitalized patients.
Medications— Medications to control difficult behavior are only to be considered as a last resort, if the patient’s agitation is so extreme as to be a potential source of harm. Some classes of drugs, especially sedatives such as lorazepam and diazepam, can build up in the bloodstream and cause the person to become more confused. Antipsychotic medications, such as haloperidol, may be considered, but only in small doses and for short periods of time. If necessary, these medications should be stopped frequently, with direction or approval by the physician, so that the patient can be reevaluated. Antipsychotic medications are not recommended for long-term treatment.
Pharmacological Parameters for Medications Used To Manage Symptoms of Delirium
Generic name
Suggested dosing
Breakthrough dosing based on tCmax
Approximate elimination t½
Recommended dosing interval
FDA-recommended maximum daily dosages
Median lethal dose in rats (LD50)
Haloperidol
Start with 1–2 mg, then use the titration technique
PO/PR: 60 min
SC/IM: 30 min
IV: 15 min
21 hr
Daily or twice daily
100 mg/day
128 mg/kg
Chlorpromazine
Start with 25–50 mg, then use the titration technique
PO/PR: 60 min
SC/IM: 30 min
IV: 15 min
24 hr
Daily or twice daily
2000 mg/day
142 mg/kg
Lorazepam
Start with 1–2 mg, then use the titration technique
0.1 to 0.2 mg/kg loading dose repeated every 30 min until symptom control, then 25% of the total dose needed to control symptoms as a continuous infusion
SC/IM: 30 min
IV: 15 min
2 hr
Continuous infusion
240 mg/day
215 mg/kg
Phenobarbital
PO/PR: Start with 30–120 mg/day in two to three divided doses; SC/IV: 10–30 mg/kg loading dose, then 20–100 mg/hr continuous infusion
Did not show improvement in condition;
treatment limited by adverse effects[rx]
Cholinesterase inhibitors
Donepezil
5 mg QD
Nausea, vomiting, diarrhea
No randomized, controlled studies have been
conducted; some case studies have indicated
promise[rx–rx]
Prophylactic therapies (potential)
Antipsychotics
Haloperidol
0.5–1 mg PO or IM; can
repeat every 4h (PO) or
every 60 min (IM)
Extrapyramidal syndrome,
prolonged QT interval
Use in surgical cases may reduce delirium
incidence;[rx] needs to be confirmed in additional
studies
Cholinesterase inhibitors
Donepezil
5 mg QD
Nausea, vomiting, diarrhea
Prevention studies have not demonstrated
efficacy[rx,rx]
Antipsychotics are the most widely used drugs for the treatment of delirium-related agitation but can have marked adverse effects.
Benzodiazepines should be reserved for treatment of drug withdrawal, diffuse Lewy body disease, or as second-line treatment following failure of antipsychotics.
Not currently accepted clinical therapies
Abbreviations: BID, twice daily; IM, intramuscularly; PO, per os (by mouth); QD, once daily.
First-Generation Antipsychotics
For the first-line treatment of a potentially reversible, hyperactive delirium, evidence supports, and published guidelines recommend, the use of first-generation antipsychotics, e.g., haloperidol and chlorpromazine. (These guidelines do not distinguish potentially reversible from irreversible delirium, nor do they address the principal underlying diagnosis and comorbidities, prognosis, functional status, goals of care, or irreversible delirium.)[rx,rx,rx,rx]
Second-Generation Antipsychotics
No evidence currently exists for improved efficacy with atypical (second or third generation) antipsychotics.[rx,rx–rx]These medications are often more expensive and have fewer routes of administration.[rx] Existing treatment guidelines suggest starting with first-generation antipsychotics.[rx]
Alpha-2 agonists
Alpha-2 agonist medication uses have been shown to be effective in decreasing the incidence of delirium in critically ill patients. These agents cause minimal respiratory depression and help in maintaining a low heart rate. Therefore, they facilitate minimal hemodynamic fluctuations and lower energy expenditure that might result in global cerebral insult.[rx] Further, alpha-2 agonists may inhibit the release and production of neurotoxic glutamate, thereby having a neuroprotective effect.[rx]
Opioids
Likewise, opioids have no role in the treatment of agitation or delirium. These are analgesics with no anti-agitation actions. Sedation is a side effect of opioids (not a therapeutic effect), and is not reliable from patient to patient or opioid to opioid. Care should be taken to differentiate pain-related behaviors from delirium-induced behaviors.
Benzodiazepines
These function as sedatives, anxiolytics – skeletal muscle relaxants, amnestics, and potent antiepileptics. Using the titration technique[rx] discussed above, the minimum benzodiazepine dose needed to rapidly and safely relieve symptoms can be established. The dose of a benzodiazepine typically needed to control the symptoms of delirium is far below their median lethal dosages.[rx,rx]
Olanzapine an atypical antipsychotic – has also been tested as a prophylactic agent to prevent postoperative delirium. 495 elderly patients undergoing elective knee or hip replacement were either assigned to a placebo arm or a treatment arm of 10mg of oral olanzapine. The treatment group had a significantly decreased incidence of delirium, but those patients who did suffer delirium had a longer, more severe course [rx].
Donepezil – a cholinesterase inhibitor FDA-approved for the treatment of Alzheimer’s disease, has also been tried as a prophylactic agent for delirium. Eighty patients were randomized to receive donepezil 14 days prior to and 14 days after surgery. There was no significant difference in the two groups [rx].
Nonpharmacological Approaches
Following are example of environmental interventions
Engage patients in mentally stimulating activities to help them with disordered thinking
Provide orienting and familiar materials to help patients know the time and date, where they are, and which staff are working with them.
Ensure all individuals identify themselves each time they encounter the patient, even if the encounters are minutes apart.
Minimize the number of people interacting with the patient and the quantity of stimulation the patient receives, e.g., television or loud music
Use family or volunteers as constant companions to help reassure and reorient a delirious patient. Encourage staff to sit with the patient while they do their documentation
Provide adequate soft lighting so patients can see without being overstimulated by bright lights.
Manage fall risks.
Provide warm milk, massage, warm blankets, and use relaxation tapes to optimize sleep hygiene and minimize sleep disturbances.
Ensure patients use their glasses, hearing aids, etc., to optimize orientation, decrease confusion, and promote better communication.
Ensure patients have good nutrition and an effective bowel and bladder management strategy.
Monitor fluid intake. Rehydrate with oral fluids containing salt, e.g., soups, sport drinks, red vegetable juices. When necessary, infuse fluids subcutaneously rather than intravenously.[rx–rx]
Use physical restraints only as a last resort to temporarily ensure the safety of both staff and a severely agitated and not redirectable patient,[rx,rx] and only until less restrictive interventions are possible.
Provide education and support to help family members cope with what they are witnessing.[rx]
Complications
Seizures
Disorientation
Hypertension
Hyperthermia
Altered mental status
Global confusion
Arrhythmias
Aspiration pneumonitis
Respiratory failure
Death
To prevent relapse, the patient should be referred to alcoholic anonymous and other support groups.
Cognitive behavior therapy may help some patients prevent relapse
A referral to a psychiatrist to assess for depression and anxiety may help abstain from alcohol.
These tips may help
Provide a reassuring environment for the patient, such as a quiet, well-lit room with familiar people and objects. It may also help to place a clock and wall calendar where a patient can see it.
Talk with the doctor, nurse, or another member of the health care team about a patient’s hallucinations or unusual behaviors. The health care team can help you learn what to expect and how to manage these symptoms.
Ask about stopping or switching medications that may worsen a patient’s mental confusion. Also, ask if there are other, untreated medical conditions that may be the cause of delirium.
In some cases, giving antipsychotic medications helps control the symptoms of delirium. Although these drugs can have side effects, most can be managed well.
Conjunctivitis Treatment/Conjunctivitis is any inflammation of the conjunctiva, generally characterised by irritation, itching, foreign body sensation, and watering or discharge. Treatment is often based on clinical suspicion that the conjunctivitis is bacterial, without waiting for the results of microbiological tests. In this review, therefore, we have distinguished the effects of empirical treatment from effects of treatment in people with culture-positive bacterial conjunctivitis. Bacterial conjunctivitis in contact lens wearers is of particular concern because of the risk of bacterial keratitis — an infection of the cornea accompanying acute or subacute corneal trauma, which is more difficult to treat than conjunctivitis and can threaten vision.
Conjunctivitis Types
1. Accordinf to the causes
Conjunctivitis may be classified either by cause or by extent of the inflamed area.
Allergy
Bacteria
Viruses
Chemicals
Autoimmune
Neonatal conjunctivitis is often grouped separately from bacterial conjunctivitis because it is caused by different bacteria than the more common cases of bacterial conjunctivitis.
2. By extent of involvement
Blepharoconjunctivitis – is the dual combination of conjunctivitis with blepharitis (inflammation of the eyelids).
Keratoconjunctivitis – is the combination of conjunctivitis and keratitis (corneal inflammation).
Blepharokeratoconjunctivitis – is the combination of conjunctivitis with blepharitis and keratitis. It is clinically defined by changes of the lid margin, meibomian gland dysfunction, redness of the eye, conjunctival chemosis and inflammation of the cornea.[rx]
3. Etiological
Simple Allergic Conjunctivitis – Most cases are secondary to simple allergen exposure on the ocular surface.
Vernal Keratoconjunctivitis – Exact etiology is not well understood but some combination of climate and allergen is believed to be responsible.
Atopic Keratoconjunctivitis – Etiology is not clear but appears to be a combination of allergen exposure, atopic dermatitis (more than 90% of cases) andor genetic predisposition.
Giant Papillary Conjunctivitis – Allergen exposure and subsequent response secondary to the ocular foreign body either harboring allergens on its surface or injuring ocular structures which facilitate allergen infiltration. It can be seen with many different ocular foreign bodies (eg., contact lenses, prostheses, cyanoacrylate glue, sutures).
Allergic conjunctivitis – This pink eye caused by eye allergies is very common. Eye allergies, like other types, can be triggered by allergens including pollen, animal dander and dust mites. The most common symptom of allergic conjunctivitis is itchy eyes, which may be relieved with special eye drops containing antihistamines to control allergic reactions. Avoiding the allergen is also important in the treatment of allergic conjunctivitis. Allergic conjunctivitis can be seasonal or perennial (year-round), depending on the allergen causing the reaction.
Giant papillary conjunctivitis – This pink eye usually impacts both eyes and often affects soft contact lens wearers. This condition may cause contact lens intolerance, itching, a heavy discharge, tearing and red bumps on the underside of the eyelids. You’ll need to stop wearing your contact lenses, at least for a little while. Your eye doctor may also recommend that you switch to a different type of contact lens, to reduce the chance of the conjunctivitis coming back.
Non-infectious conjunctivitis – This conjunctivitis from eye irritation causing pink eye symptoms that can result from many sources, including smoke, diesel exhaust, perfumes and certain chemicals. Some forms of conjunctivitis also result from sensitivity to certain ingested substances, including herbs such as eyebright and turmeric.
Pathophysiology
Regardless of the etiology, most cases of conjunctivitis can be categorized as either papillary or follicular. Neither classification is pathognomonic for a particular disease entity. Papillary conjunctivitis produces a cobblestone arrangement of flattened nodules with central vascular cores. It is most commonly associated with an allergic immune response or is a response to a foreign body. Independent of the etiology, the histologic appearance of papillary conjunctivitis is the same: closely packed, flat-topped projections, with numerous eosinophils, lymphocytes, plasma cells, and mast cells in the stroma surrounding a central vascular channel.
Follicular conjunctivitis is seen in a variety of conditions, including inflammation caused by pathogens such as viruses, bacteria, toxins, and topical medications. In contrast to papillae, follicles are small, dome-shaped nodules without a prominent central vessel. Histologically, a lymphoid follicle is situated in the subepithelial region and consists of a germinal centerwith immature, proliferating lymphocytes surrounded by a ringof mature lymphocytes and plasma cells. The follicles in follicular conjunctivitis are typically most prominent in the inferior palpebral and forniceal conjunctiva.[rx]
Epidemiology
Simple Allergic Conjunctivitis – It is difficult to estimate how many patients are affected as the symptoms are often under-appreciated, and many patients go without seeking medical care. Simple ocular allergy likely affects between 10% to 30% of the general population. In most cases, onset occurs in patients younger than 20 years old with decreasing prevalence in older populations. Allergic conjunctivitis can be seen as an isolated finding but is often associated with allergic rhinitis, atopic dermatitis, and/or asthma.
Vernal Keratoconjunctivitis – More commonly seen in males (ratio 2:1 to 3:1) in dry, warm climates. Most cases occur in patients younger than ten who often have a history of atopy or asthma. Many patients have complete resolution without the return of symptoms after adolescence.
Atopic Keratoconjunctivitis – Not usually seen before adolescence and peaks from 30 to 50 years of age. Most cases are seen in patients with atopic dermatitis. Like vernal keratoconjunctivitis, there is a male to female predominance
Giant Papillary Conjunctivitis – Seen most commonly in teens and young adults, most likely because of a temporal relationship with contact lens use. Most commonly seen in conjunction with soft contact lens use and is present in approximately 5% of that population. Average onset is one to two years after starting soft contact lenses but varies widely with other ocular foreign bodies.[rx][rx][rx]
Conjunctivitis Causes
Infective conjunctivitis is most commonly caused by a virus.[rx] Bacterial infections, allergies, other irritants, and dryness are also common causes. Both bacterial and viral infections are contagious, passing from person to person or spread through contaminated objects or water. Contact with contaminated fingers is a common cause of conjunctivitis. Bacteria may also reach the conjunctiva from the edges of the eyelids and the surrounding skin, from the nasopharynx, from infected eye drops or contact lenses, from the genitals or the bloodstream.[rx] Infection by human adenovirus accounts for 65% to 90% of cases of viral conjunctivitis.[rx]
Viral – Adenoviruses are the most common cause of viral conjunctivitis (adenoviral keratoconjunctivitis).[rx] Herpetic keratoconjunctivitis, caused by herpes simplex viruses, can be serious and requires treatment with aciclovir. Acute hemorrhagic conjunctivitis is a highly contagious disease caused by one of two enteroviruses, enterovirus 70 and coxsackievirus A24. These were first identified in an outbreak in Ghana in 1969, and have spread worldwide since then, causing several epidemics.[rx]
Pharyngoconjunctival fever – Which is common, mild and often seen in children and young adults who have recently had a cold or respiratory infection. Symptoms may include sore throat, fever and headache.
Epidemic keratoconjunctivitis – Which is less common, can be severe, affects the front of the eye (cornea) and may cause long-lasting vision difficulties. Also known as viral keratoconjunctivitis. Less common causes of viral conjunctivitis include
Enteroviruses
Herpes simplex virus, the cold sore virus, which usually affects only one eye
Herpes zoster ophthalmicus, associated with shingles
Molluscum contagiosum, also known as water warts
Measles
Mumps
Rubella, also known as German measles
Infectiou
Bacterial – The most common causes of acute bacterial conjunctivitis are Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae.[rx][rx] Though very rare, hyperacute cases are usually caused by Neisseria gonorrhoeae or Neisseria meningitidis. Chronic cases of bacterial conjunctivitis are those lasting longer than 3 weeks, and are typically caused by S. aureus, Moraxella lacunata, or Gram-negative enteric flora.
Allergic –Conjunctivitis may also be caused by allergens such as pollen, perfumes, cosmetics, smoke,[rx] dust mites, Balsam of Peru,[rx] or eye drops.[rx] The most frequent cause of conjunctivitis is allergic conjunctivitis and it affects 15% to 40% of the population.[rx] Allergic conjunctivitis accounts for 15% of eye related primary care consultations – most including seasonal exposures in the spring and summer or perpetual conditions. [rx]
Blepharitis – This is a common inflammation of the eyelids that causes redness, irritation, and itching. There will also be dandruff-like scales on the eyelashes. Blepharitis is not contagious.
Acute glaucoma – This is a rare form of glaucoma, in which pressure builds up in the eye. Symptoms can appear quickly and include pain, red eyes, and vision loss, which may become permanent without treatment.
Keratitis – The cornea becomes inflamed and possibly ulcerated. If scarring of the cornea occurs, this can lead to permanent loss of vision. The cornea is the transparent part at the front of the eye.
Iritis – The iris becomes inflamed. Untreated iritis can cause the iris to become stuck to the front surface of the lens, preventing fluid draining from the pupil. This can eventually lead to permanent eye damage. The iris is the colored part of the eye, the part that controls the amount of light that enters into the eye.
Other – Conjunctivitis is part of the triad of reactive arthritis, which is thought to be caused by autoimmune cross-reactivity following certain bacterial infections. Reactive arthritis is highly associated with HLA-B27. Conjunctivitis is associated with the autoimmune disease relapsing polychondritis.[rx][rx]
Selected Nonconjunctivitis Causes of Red Eye
Differential Diagnosis
Symptoms
Penlight Examination Findings
Dry eye disease
Burning and foreign-body sensation. Symptoms are usu-
ally transient, worse with prolonged reading or watching
television because of decreased blinking. Symptoms are
worse in dry, cold, and windy environments because of
increased evaporation.
Bilateral redness
Blepharitis
Similar to dry eyes
Redness greater at the margins of eyelids
Uveitis
Photophobia, pain, blurred vision. Symptoms are usually
bilateral.
Decreased vision, poorly reacting pupils, constant eye
pain radiating to temple and brow. Redness,
severe photophobia, presence of inflammatory cells in
the anterior chamber.
Angle closure glaucoma
Headaches, nausea, vomiting, ocular pain, decreased
vision, light sensitivity, and seeing haloes around lights.
Symptoms are usually unilateral.
Firm eye on palpation, ocular redness with limbal injec-
tion. Appearance of a hazy/steamy cornea, moderately
dilated pupils that are unreactive to light.
Carotid cavernous fistula
Chronic red eye; may have a history of head trauma
Dilated tortuous vessels (corkscrew vessels), bruits on
auscultation with a stethoscope
Endophthalmitis
Severe pain, photophobia, may have a history of eye sur-
gery or ocular trauma
Redness, pus in the anterior chamber, and
photophobia
Cellulitis
Pain, double vision, and fullness
Redness and swelling of lids, may have restriction of the
eye movements, may have a history of preceding sinus-
itis (usually ethmoiditis)
Anterior segment tumors
Variable
Abnormal growth inside or on the surface of the eye
Scleritis
Decreased vision, moderate to severe pain
Redness, bluish sclera hue
Subconjunctival hemorrhage
May have foreign-body sensation and tearing or be
asymptomatic
Blood under the conjunctival membrane
Data are from Cronau et al[rx] and Leibowitz.[rx] The examination can be done by shining a penlight in the patient’s affected eye(s).
Conjunctivitis Symptoms
Pink or red color in the white of the eye(s)
Swelling of the conjunctiva (the thin layer that lines the white part of the eye and the inside of the eyelid) and/or eyelids
Increased tear production
Feeling like a foreign body is in the eye(s) or an urge to rub the eye(s)
Itching, irritation, and/or burning
Discharge (pus or mucus)
Crusting of eyelids or lashes, especially in the morning
Contact lenses that feel uncomfortable and/or do not stay in place on the eye
Depending on the cause, other symptoms may occur.
Viral Conjunctivitis
Can occur with symptoms of a cold, flu, or other respiratory infection
Usually begins in one eye and may spread to the other eye within days
Discharge from the eye is usually watery rather than thick
Bacterial Conjunctivitis
More commonly associated with discharge (pus), which can lead to eyelids sticking together
Sometimes occurs with an ear infection
Allergic Conjunctivitis
Usually occurs in both eyes
Can produce intense itching, tearing, and swelling in the eyes
May occur with symptoms of allergies, such as an itchy nose, sneezing, a scratchy throat, or asthma
Overall Symptoms
They depend on the cause of the inflammation, but may include:
Comparison of key clinical characteristics between viral, bacterial and self-inflicted conjunctivitis
Clinical characteristics/Etiology
Bacterial
Viral
Self-inflicted
Duration
Can be prolonged without treatment. Treatment hastens recovery
Days to weeks
Can be prolonged. Weeks to months
Bilateral/unilateral
Usually spreads to the other eye within days
Usually spreads to the other eye within days
Varies
Type of discharge
Mostly purulent discharge
Mostly aqueous, possibly mucoid discharge
Tearing and excessive discharge, fresh and dry purulent discharge on eyelids and periorbital skin
Swollen lymph glands
Not common
Common
Not common
Concomitant signs
None
Pyrexia , pharyngitis
Emotional or social stress, multiple physical complaints
Complications
Uncommon
Uncommon
Uncommon
Additional findings
Ocular irritation
Diffuse conjunctival involvement. Foreign body sensation
Mainly involvement of the lower conjunctiva. Discharge and edema are conspicuously prominent in relation to the conjunctival hyperemia
Response to treatment
Usually subsides without treatment.
Usually subsides without treatment.
Non-responsive to treatment
Responds well to antibiotics
Epidemiological characteristics
Contagious. Can lead to an outbreak
Very contagious. Can lead to an outbreak
Rarely the cause of an outbreak. Is usually diagnosed in a single soldier for secondary gain and not in a cluster
Diagnosis of Conjunctivitis
History and Physical – Allergic conjunctivitis frequently accompanies seasonal allergy symptoms, specifically known allergy exposures or a history of atopy. As such, recurrent episodes are commonly seen. Practitioners should elicit a personal history of allergies and atopy, as well as, a history of similar episodes in the past. Practitioners should ask about specific symptoms from the current and any past episodes. Itchiness and diffuse bulbar and tarsal conjunctival injection are the most commonly reported symptoms and are present in all subtypes of allergic conjunctivitis. Other histories and physical exam findings vary with the specific subtype of allergic conjunctivitis.
Simple Allergic Conjunctivitis – Clear, watery discharge is the most commonly seen discharge and is usually bilateral with minimal crusting in the mornings. Pain and decreased visual acuity are not commonly reported in simple allergic conjunctivitis and should prompt the provider to consider another diagnosis. Eyelid edema and chemosis are not uncommon and can be quite marked.
Vernal Keratoconjunctivitis – Symptoms are usually most severe in the spring and include thick mucus discharge, pain, photophobia and blurred vision. Patients will also often complain of foreign body sensation. On examination, corneal ulcers and conjunctival infiltrates can sometimes be found. Giant papillae on the tarsal conjunctiva are universally seen on examination.
Atopic Keratoconjunctivitis – Symptoms are usually perennial and include pain, blurry vision, photophobia and foreign body sensation. Examination reveals findings similar to simple allergic conjunctivitis with the addition of chronic inflammatory changes to the ocular surface (corneal scarring and neovascularization) and varied changes to the eyelids (lower lid more commonly) and peri-orbital skin that range from mild atopy to lichenification.
Giant Papillary Conjunctivitis – Symptoms consistent with simple allergic conjunctivitis often give way to worsening itch and discharge that becomes thick mucus instead of clear and watery. Patients usually report worsening pain and blurry vision with the increased sense of foreign body (contact lenses, sutures). The examination reveals findings consistent with simple allergic conjunctivitis as well as giant papillae covering the tarsal conjunctiva.
Selected Nonconjunctivitis Causes of Red Eye
Differential Diagnosis
Symptoms
Penlight Examination Findings
Dry eye disease
Burning and foreign-body sensation. Symptoms are usu-
ally transient, worse with prolonged reading or watching
television because of decreased blinking. Symptoms are
worse in dry, cold, and windy environments because of
increased evaporation.
Bilateral redness
Blepharitis
Similar to dry eyes
Redness greater at the margins of eyelids
Uveitis
Photophobia, pain, blurred vision. Symptoms are usually
bilateral.
Decreased vision, poorly reacting pupils, constant eye
pain radiating to temple and brow. Redness,
severe photophobia, presence of inflammatory cells in
the anterior chamber.
Angle closure glaucoma
Headaches, nausea, vomiting, ocular pain, decreased
vision, light sensitivity, and seeing haloes around lights.
Symptoms are usually unilateral.
Firm eye on palpation, ocular redness with limbal injec-
tion. Appearance of a hazy/steamy cornea, moderately
dilated pupils that are unreactive to light.
Carotid cavernous fistula
Chronic red eye; may have a history of head trauma
Dilated tortuous vessels (corkscrew vessels), bruits on
auscultation with a stethoscope
Endophthalmitis
Severe pain, photophobia, may have a history of eye sur-
gery or ocular trauma
Redness, pus in the anterior chamber, and
photophobia
Cellulitis
Pain, double vision, and fullness
Redness and swelling of lids, may have restriction of the
eye movements, may have a history of preceding sinus-
itis (usually ethmoiditis)
Anterior segment tumors
Variable
Abnormal growth inside or on the surface of the eye
Scleritis
Decreased vision, moderate to severe pain
Redness, bluish sclera hue
Subconjunctival hemorrhage
May have foreign-body sensation and tearing or be
asymptomatic
Blood under the conjunctival membrane
Data are from Cronau et al[rx] and Leibowitz.[rx] The examination can be done by shining a penlight in the patient’s affected eye(s).
GRADE evaluation of interventions for bacterial conjunctivitis.
Important outcomes
Cure rates, adverse effects
Number of studies (participants)
Outcome
Comparison
Type of evidence
Quality
Consistency
Directness
Effect size
GRADE
Comment
What are the effects of empirical treatment in adults and children with suspected bacterial conjunctivitis?
8 (2515)
Cure rates
Topical antibiotics vplacebo or no immediate treatment
4
−1
−1
0
0
Low
Quality point deducted for self-report of clinical cure by parents in 1 RCT. Consistency point deducted for conflicting results
24 (at least 2754)
Cure rates
Topical antibiotics veach other
4
−2
0
0
0
Low
Quality points deducted for incomplete reporting of results and for weak methods in some RCTs
1 (80)
Cure rates
Topical voral antibiotics
4
−2
0
−1
0
Very low
Quality points deducted for sparse data and incomplete reporting of results. Directness point deducted for small number of comparators
1 (104)
Cure rates
Different regimens of topical antibiotics veach other
4
−1
0
−1
0
Low
Quality point deducted for sparse data. Directness point deducted for small number of comparators
What are the effects of treatment in adults and children with bacteriologically confirmed bacterial conjunctivitis?
8 (1933)
Cure rates
Topical antibiotics vplacebo
4
0
0
−1
0
Moderate
Directness point deducted for uncertainty about generalisability of results (to situations where treatment not initiated until culture results are known, because of the delay in treatment)
9 (at least 1584)
Cure rates
Topical antibiotics v each other
4
−1
−1
0
0
Low
Quality point deducted for incomplete reporting of results. Consistency point deducted for inconsistent results between RCTs
1 (86)
Cure rates
Different regimens of topical antibiotics veach other
4
−1
0
−1
0
Low
Quality point deducted for sparse data. Directness point deducted for small number of comparators
What are the effects of treatment in adults and children with clinically confirmed gonococcal conjunctivitis?
4 (239)
Cure rates
Parenteral antibiotics plus topical antibiotics vparenteral antibiotics alone or vparenteral antibiotics plus different topical antibiotic
4
−1
−1
−1
0
Very low
Quality point deducted for incomplete reporting of results. Consistency point deducted for conflicting results. Directness point deducted for all studies in Africa, which may affect generalisability
Type of evidence: 4 = RCT. Consistency: similarity of results across studies. Directness: generalisability of population or outcomes. Effect size: based on relative risk or odds ratio.
Treatment of
The appropriate treatment for conjunctivitis depends on its cause:
Allergic conjunctivitis – The first step is to remove or avoid the irritant, if possible. Cool compresses and artificial tears sometimes relieve discomfort in mild cases. In more severe cases, nonsteroidal anti-inflammatory medications and antihistamines may be prescribed. People with persistent allergic conjunctivitis may also require topical steroid eye drops.
Bacterial conjunctivitis – This type of conjunctivitis is usually treated with antibiotic eye drops or ointments. Bacterial conjunctivitis may improve after three or four days of treatment, but patients need to take the entire course of antibiotics to prevent recurrence.
Viral conjunctivitis – No drops or ointments can treat viral conjunctivitis. Antibiotics will not cure a viral infection. Like a common cold, the virus has to run its course, which may take up to two or three weeks. Symptoms can often be relieved with cool compresses and artificial tear solutions. For the worst cases, topical steroid drops may be prescribed to reduce the discomfort from inflammation. However, these drops will not shorten the infection.
Chemical conjunctivitis – Careful flushing of the eyes with saline is a standard treatment for chemical conjunctivitis. People with chemical conjunctivitis also may need to use topical steroids. Severe chemical injuries, particularly alkali burns, are medical emergencies and can lead to scarring, damage to the eye or the sight, or even loss of the eye. If a chemical spills in your eye, flush the eye for several minutes with a lot of water before seeing your medical provider.
Topical antibiotics used to treat bacterial conjunctivitis
Antibiotic
Class
Coverage
Mechanism
Availability
Azithromycin
Macrolide
Broad-spectrum
Baceriostatic
Azasite® 1% (Inspire Pharmaceuticals Inc)
Besifloxacin
Fluoroquinolone
Broad-spectrum
Bactericidal
Besivance® 0.6% (Bausch and Lomb)
Chloramphenicol
Chloramphenicol
Broad-spectrum
Bacteriostatic
Topical drops not marketed in US
Optrex Infected Eyes® 0.5% in UK
Ciprofloxacin
Fluoroquinolone
Broad-spectrum
Bactericidal
Ciloxan® 0.3% (Alcon Laboratories Inc)
Ointment or drops
Fusidic acid
Protein synthesis inhibitor
Primarily Gram-positive
Bacteriostatic
Not available in US
Fucithalmic® 1% (Leo Pharma) in Canada and UK
Gatifloxacin
Fluoroquinolone
Broad-spectrum
Bactericidal
Zymar 0.3% (Allergan Inc)
Gentamicin
Aminoglycoside
Primarily Gram-negative
Bactericidal
Generic 0.3% drops
Levofloxacin
Fluoroquinolone
Broad-spectrum
Bactericidal
Iquix® 1.5% (Vistakon Pharmaceuticals)
Lomefloxacin
Fluoroquinolone
Broad-spectrum
Bactericidal
Not available in US
Moxifloxacin
Fluoroquinolone
Broad-spectrum
Bactericidal
Vigamox® 0.5% (Alcon Laboratories Inc)
Neomycin-polymyxin B-gramicidin
Aminoglycoside, polymyxin and gramicidin
Broad-spectrum
Bactericidal
Neosporin® (King Pharmaceuticals Inc)
Netilmicin
Aminoglycoside
Primarily Gram-negative
Bactericidal
Not available in US
Norfloxacin
Fluoroquinolone
Broad-spectrum
Bactericidal
Chibroxin 0.3% (Merck and Co Inc)
Not available in US
Ofloxacin
Fluoroquinolone
Broad-spectrum
Bactericidal
Generic 0.3% eye drops
Providone-iodine
Broad-spectrum
Bactericidal
Betadine 5% (Alcon Laboratories Inc)
Rifamycin
Rifamycin
Broad-spectrum
Bactericidal
Not available in US
Tobramycin
Aminoglycoside
Primarily Gram-negative
Bactericidal
Tobrex® 0.3% (Alcon Laboratories Inc) ointment or drops
Alternatives to Immediate Antibiotic Therapy
To our knowledge, no studies have been conducted to evaluate the efficacy of ocular decongestant, topical saline, or warm compresses for treating bacterial conjunctivitis.[rx] Topical steroids should be avoided because of the risk of potentially prolonging the course of the disease and potentiating the infection.[rx]
Summary of Recommendations for Managing Bacterial Conjunctivitis
In conclusion, benefits of antibiotic treatment include quicker recovery, decrease in transmissibility,[rx] and early return to school.[rx]Simultaneously, adverse effects are absent if antibiotics are not used in uncomplicated cases of bacterial conjunctivitis. Therefore, no treatment, a wait-and-see policy, and immediate treatment all appear to be reasonable approaches in cases of uncomplicated conjunctivitis. Antibiotic therapy should be considered in cases of purulent or mucopurulent conjunctivitis and for patients who have distinct discomfort, who wear contact lenses,[rx,rx] who are immunocompromised, and who have suspected chlamydial and gonococcal conjunctivitis.
Special Topics in Bacterial Conjunctivitis
Methicillin-Resistant S aureus Conjunctivitis
It is estimated that 3% to 64% of ocular staphylococcal infections are due to methicillin-resistant S aureus conjunctivitis; this condition is becoming more common and the organisms are resistant to many antibiotics.[rx] Patients with suspected cases need to be referred to an ophthalmologist and treated with fortified vancomycin.[rx]
Chlamydial Conjunctivitis
It is estimated that 1.8% to 5.6% of all acute conjunctivitis is caused by chlamydia,[rx–rx] and the majority of cases are unilateral and have concurrent genital infection.[rx]Conjunctival hyperemia, mucopurulent discharge, and lymphoid follicle formation[rx] are hallmarks of this condition. Discharge is often purulent or mucopurulent.[rx] How ever, patients more often present with mild symptoms for weeks to months. Up to 54% of men and 74% of women have concurrent genital chlamydial infection.[rx] The disease is often acquired via oculogenital spread or other intimate contact with infected individuals; in newborns the eyes can be infected after vaginal delivery by infected mothers.[rx] Treatment with systemic antibiotics such as oral azithromycin and doxycycline is efficacious; patients and their sexual partners must be treated and a coinfection with gonorrhea must be investigated. No data support the use of topical antibiotic therapy in addition to systemic treatment.[rx] Infants with chlamydial conjunctivitis require systemic therapy because more than 50% can have concurrent lung, nasopharynx, and genital tract infection.[rx]
Gonococcal Conjunctivitis
Conjunctivitis caused by N gonorrhoeae is a frequent source of hyperacute conjunctivas in neonates and sexually active adults and young adolescents.[rx] Treatment consists of both topical and oral antibiotics. Neisseria gonorrhoeae is associated with a high risk of cor-neal perforation.[rx]
Conjunctivitis Secondary to Trachoma
Trachoma is caused by Chlamydia trachomatis subtypes A through C and is the leading cause of blindness, affecting 40 million people worldwide in areas with poor hygiene.[rx,rx] Mucopurulent discharge and ocular discomfort may be the presenting signs and symptoms in this condition. Late complications such as scarring of the eyelid, conjunctiva, and cornea may lead to loss of vision. Treatment with a single dose of oral azithromycin (20 mg/kg) is effective. Patients may also be treated with topical antibiotic ointments for 6 weeks (ie, tetracycline or erythromycin). Systemic antibiotics other than azithromycin, such as tetracycline or erythromycin for 3 weeks, may be used alternatively.[rx,rx]
Ophthalmic Therapies for Conjunctivitis
Category
Epidemiology
Type of
Discharge
Cause
Treatment
Level of Evidence
for Treatment
Acute bacterial
conjunctivitis
135 case per 10 000
population in US[rx]
18.3%-57% of all acute
conjunctivitis[rx–rx,rx,rx]
Mucopurulent
S aureus, S epidermidis, H influenzae, S pneumoniae, S viridans, Moraxellaspp
Aminoglycosides
Gentamicin
Ointment: 4 ×/d for 1 wk
Solution: 1-2 drops 4 ×/d for 1 wk
Abbreviations: IM, intramuscularly; NA, not available; NSAIDs, nonsteroidal anti-inflammatory drugs.
Allergic Conjunctivitis
Prevalence and Cause
Allergic conjunctivitis is the inflammatory response of the conjunctiva to allergens such as pollen, animal dander, and other environmental antigens[rx] and affects up to 40% of the population in the United States[rx]; only about 10% of individuals with allergic conjunctivitis seek medical attention, and the entity is often underdiagnosed.[rx] Redness and itching are the most consistent symptoms.[rx]Seasonal allergic conjunctivitis comprises 90% of all allergic conjunctivitis in the United States.[rx
Drug-, Chemical-, and Toxin-Induced Conjunctivitis
A variety of topical medications such as antibiotic eyedrops, topical antiviral medications, and lubricating eyedrops can induce allergic conjunctival responses largely because of the presence of benzalkonium chloride in eye drop preparations.[rx] Cessation of receiving the offending agent leads to resolution of symptoms.[rx]
Systemic Diseases Associated With Conjunctivitis
A variety of systemic diseases, including mucous membrane pemphigoid, Sjögren syndrome, Kawasaki disease,[rx] Stevens-Johnson syndrome,[rx] and carotid cavernous fistula,[rx] can present with signs and symptoms of conjunctivitis, such as conjunctival redness and discharge. Therefore, the above causes should be considered in patients presenting with conjunctivitis. For example, patients with low-grade carotid cavernous fistula can present with chronic conjunctivitis recalcitrant to medical therapy, which, if left untreated, can lead to death.
Ominous Signs
As recommended by the American Academy of Ophthalmology,[rx] patients with conjunctivitis who are evaluated by nonophthalmologist health care practitioners should be referred promptly to an ophthalmologist if any of the following develops: visual loss, moderate or severe pain, severe purulent discharge, corneal involvement, conjunctival scarring, lack of response to therapy, recurrent episodes of conjunctivitis, or history of herpes simplex virus eye disease. In addition, the following patients should be considered for referral: contact lens wearers, patients requiring steroids, and those with photophobia. Patients should be referred to an ophthalmologist if there is no improvement after 1 week.[x]
Importance of Not Using Antibiotic/Steroid Combination Drops
Steroid drops or combination drops containing steroids should not be used routinely. Steroids can increase the latency of the adeno-viruses, the refore prolonging the course of viral conjunctivitis. In addition, if an undiagnosed corneal ulcer secondary to herpes, bacteria, or fungus is present, steroids can worsen the condition, leading to corneal melt and blindness.
Randomized controlled trials comparing antibiotics with placebo
One group received besifloxacin
One group received “vehicle”
Clinical resolution and bacterial eradication
Higher rate of microbial and clinical cure with antibiotic
Prevention
Here are nine simple precautions you can take to significantly reduce your risk of getting pink eye:
Never share personal items – such as washcloths, hand towels or tissues.
Cover your nose and mouth – when coughing or sneezing, and avoid rubbing or touching your eyes.
Wash your hands frequently – especially when spending time at school or in other public places.
Keep a hand sanitizer nearby – and use it frequently.
Frequently clean – surfaces such as countertops, bathroom surfaces, faucet handles and shared phones with an antiseptic cleaner.
If you know you suffer from seasonal allergies – ask your doctor what can be done to minimize your symptoms before they begin.
If you wear contact lenses – follow your eye doctor’s instructions for lens care and replacement, and use contact lens solutions properly or consider switching to daily disposable contact lenses.
When swimming – wear swim goggles to protect yourself from bacteria and other microorganisms in the water that can cause conjunctivitis.
Before showering -remove your contact lenses to avoid trapping bacteria between your eyes and the lenses.
To help you cope with the signs and symptoms of pink eye until it goes away, try to
Apply a compress to your eyes. To make a compress, soak a clean, lint-free cloth in water and wring it out before applying it gently to your closed eyelids. Generally, a cool water compress will feel the most soothing, but you can also use a warm compress if that feels better to you. If pink eye affects only one eye, don’t touch both eyes with the same cloth. This reduces the risk of spreading pink eye from one eye to the other.
Try eyedrops. Over-the-counter eyedrops called artificial tears may relieve symptoms. Some eyedrops contain antihistamines or other medications that can be helpful for people with allergic conjunctivitis.
Stop wearing contact lenses. If you wear contact lenses, you may need to stop wearing them until your eyes feel better. How long you’ll need to go without contact lenses depends on what’s causing your conjunctivitis. Ask your doctor whether you should throw away your disposable contacts, as well as your cleaning solution and lens case. If your lenses aren’t disposable, clean them thoroughly before reusing them.
How Much Folate Do You Need a Day/Vitamin B9 is one of the B vitamins. Folic acid is a form of vitamin B-9 that can dissolve in water. It is a key ingredient in the making of the nucleic acid that forms part of all genetic material.The recommended daily intake of folate in the US is 400 micrograms from foods or dietary supplements. Folate in the form of folic acid is used to treat anemia caused by folic acid deficiency. Folic acid is also used as a supplement by women during pregnancy to prevent neural tube defects(NTD) in the baby. Low levels in early pregnancy are believed to be the cause of more than half of babies born with neural tube defects. More than 50 countries use fortification of certain foods with folic acid as a measure to decrease the rate of NTDs in the population. Long term supplementation is also associated with small reductions in the risk of stroke and cardiovascular disease.It may be taken by mouth or by injection.
Folate, distinct forms of which are known as folic acid, folacin, and vitamin B9,[rx] is one of the B vitamins.[rx] It may be taken by mouth or by injection.[rx] The recommended adult daily intake of folate in the U.S. is 400 micrograms from foods or dietary supplements.[rx] Folate in the form of folic acid is used to treat anemia caused by folic acid deficiency.[4] Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in the baby.[4][9] Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs.[rx] More than 80 countries use fortification of certain foods with folic acid as a measure to decrease the rate of NTDs
Symptoms of Vitamin B9 Deficiency
Folic acid deficiency occurs when the newborn baby does not receive enough of this vitamin in the womb. A fetus that has received insufficient quantities of folic acid has strong possibilities of being born with spina bifida and may also suffer from serious defects of the nervous system.
Deficiency of folic acid may also lead to the following
anemia(macrocytic, megaloblastic anemia) can be a sign of advanced folate deficiency.
Women with folate deficiency who become pregnant are more likely to give birth to low birth weight premature infants, and infants with neural tube defects.
In infants and children, folate deficiency can lead to failure to thrive or slow growth rate,
diarrhea
oral ulcers
megaloblastic anemia,
neurological deterioration.
Microcephaly
seizures
blindness and cerebellar ataxia can also be observed.
Folic acid has many roles to play in the development of bones and iron uptake by the cells. Hence its deficiency may lead to malfunctioning of the vital systems.
Recommended Intakes of Vitamin B9
Intake recommendations for folate and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the Institute of Medicine (IOM) of the National Academies (formerly National Academy of Sciences) . DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values, which vary by age and gender, include:
Recommended Dietary Allowance (RDA) – Average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals; often used to plan nutritionally adequate diets for individuals.
Adequate Intake (AI) – Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA.
Estimated Average Requirement (EAR) – Average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals.
Tolerable Upper Intake Level (UL) – Maximum daily intake unlikely to cause adverse health effects.
Table 1 lists the current RDAs for folate as micrograms (mcg) of dietary folate equivalents (DFEs). The FNB developed DFEs to reflect the higher bioavailability of folic acid than that of food folate. At least 85% of folic acid is estimated to be bioavailable when taken with food, whereas only about 50% of folate naturally present in food is bioavailable . Based on these values, the FNB defined DFE as follows:
1 mcg DFE = 1 mcg food folate
1 mcg DFE = 0.6 mcg folic acid from fortified foods or dietary supplements consumed with foods
1 mcg DFE = 0.5 mcg folic acid from dietary supplements taken on an empty stomach
For infants from birth to 12 months, the FNB established an AI for folate that is equivalent to the mean intake of folate in healthy, breastfed infants in the United States.
Recommended Dietary Allowances (RDAs) for Folate
Age
Male
Female
Pregnant
Lactating
Birth to 6 months*
65 mcg DFE*
65 mcg DFE*
7–12 months*
80 mcg DFE*
80 mcg DFE*
1–3 years
150 mcg DFE
150 mcg DFE
4–8 years
200 mcg DFE
200 mcg DFE
9–13 years
300 mcg DFE
300 mcg DFE
14–18 years
400 mcg DFE
400 mcg DFE
600 mcg DFE
500 mcg DFE
19+ years
400 mcg DFE
400 mcg DFE
600 mcg DFE
500 mcg DFE
* Adequate Intake (AI)
Food Source of Vitamin B9
Selected Food Sources of Folate and Folic Acid
Food
mcg DFE
per serving
Percent DV*
Beef liver, braised, 3 ounces
215
54
Spinach, boiled, ½ cup
131
33
Black-eyed peas (cowpeas), boiled, ½ cup
105
26
Breakfast cereals, fortified with 25% of the DV†
100
25
Rice, white, medium-grain, cooked, ½ cup†
90
23
Asparagus, boiled, 4 spears
89
22
Spaghetti, cooked, enriched, ½ cup†
83
21
Brussels sprouts, frozen, boiled, ½ cup
78
20
Lettuce, romaine, shredded, 1 cup
64
16
Avocado, raw, sliced, ½ cup
59
15
Spinach, raw, 1 cup
58
15
Broccoli, chopped, frozen, cooked, ½ cup
52
13
Mustard greens, chopped, frozen, boiled, ½ cup
52
13
Green peas, frozen, boiled, ½ cup
47
12
Kidney beans, canned, ½ cup
46
12
Bread, white, 1 slice†
43
11
Peanuts, dry roasted, 1 ounce
41
10
Wheat germ, 2 tablespoons
40
10
Tomato juice, canned, ¾ cup
36
9
Crab, Dungeness, 3 ounces
36
9
Orange juice, ¾ cup
35
9
Turnip greens, frozen, boiled, ½ cup
32
8
Orange, fresh, 1 small
29
7
Papaya, raw, cubed, ½ cup
27
7
Banana, 1 medium
24
6
Yeast, baker’s, ¼ teaspoon
23
6
Egg, whole, hard-boiled, 1 large
22
6
Vegetarian baked beans, canned, ½ cup
15
4
Cantaloupe, raw, 1 wedge
14
4
Fish, halibut, cooked, 3 ounces
12
3
Milk, 1% fat, 1 cup
12
3
Ground beef, 85% lean, cooked, 3 ounces
7
2
Chicken breast, roasted, ½ breast
3
1
* DV = Daily Value. The FDA developed DVs to help consumers compare the nutrient contents of products within the context of a total diet. The DV for folate is 400 mcg for adults and children aged 4 and older. However, the FDA does not require food labels to list folate content unless a food has been fortified with this nutrient. Foods providing 20% or more of the DV are considered to be high sources of a nutrient.
† Fortified with folic acid as part of the folate fortification program.
The U.S. Department of Agriculture’s Nutrient Database Web site lists the nutrient content of many foods and provides a comprehensive list of foods containing folate arranged by nutrient content and by food name.
Serious kidney disease – About 85% of people with serious kidney disease have high levels of homocysteine. High levels of homocysteine have been linked to heart disease and stroke. Taking folic acid lowers homocysteine levels in people with serious kidney disease. However, folic acid supplementation does not appear to reduce the risk of heart disease-related events.
High amounts of homocysteine in the blood (hyperhomocysteinemia) – High levels of homocysteine have been linked to heart disease and stroke. Taking folic acid lowers homocysteine levels by 20% to 30% in people with normal to slightly elevated homocysteine levels. It is recommended that people with homocysteine levels greater than 11 micromoles/L supplement with folic acid and vitamin B12.
Reducing harmful effects of a medicine called methotrexate – Taking folic acid seems to reduce nausea and vomiting, which are possible side effects of methotrexate treatment.
Birth defects (neural tube defects) – Folic acid during pregnancy reduces the risk of neural tube birth defects. It is recommended that pregnant women get 600-800 mcg of folic acid per day from their diet or supplements starting 1 month before pregnancy and during pregnancy. Pregnant women with a history of neural tube birth defects are advised to get 4000 mcg of folic acid per day.
Possibly Effective for
Age-related vision loss (age-related macular degeneration) – Research shows that taking folic acid with other vitamins including vitamin B6 and vitamin B12 reduces the risk of developing age-related vision loss.
Depression – Limited research shows that taking folic acid along with antidepressants seems to improve symptoms in people with depression.
High blood pressure – Research shows that taking folic acid daily for at least 6 weeks reduces blood pressure in people with high blood pressure. But Taking folic acid with blood pressure medication does not seem to lower blood pressure more than taking only blood pressure medicine
Gum problems due to a drug called phenytoin – Applying folic acid to the gums seems to prevent gum problems caused by phenytoin. However, taking folic acid by mouth does not seem to improve symptoms of this condition.
Gum disease during pregnancy – Applying folic acid to the gums seems to improve gum disease during pregnancy.
Stroke – Taking folic acid can reduce the risk of stroke by 10% to 25% in people who live in countries that don’t fortify grain products with folic acid. But folic acid doesn’t seem to prevent strokes in most people who live in countries that do fortify grain products with folic acid.
A skin discoloration disorder called vitiligo – Taking folic acid by mouth seems to improve symptoms of vitiligo.
Cancer of the white blood cells (acute lymphoblastic leukemia) – Taking folate during pregnancy does not reduce the risk of childhood cancer of the white blood cells.
Iron deficiency – Taking folic acid with iron supplements is not more effective than taking the iron supplements without folic acid for treating and preventing iron deficiency and anemia caused by too little iron in the body.
Memory and thinking skills in older people – Most research shows that taking folic acid does not prevent decline in memory and thinking skills in the elderly.
Preventing re-blockage of blood vessels after angioplasty – There is inconsistent evidence on the benefits of taking folic acid after a procedure to widen the blood vessels. But taking folic acid plus vitamin B6 and vitamin B12 might actually interfere with healing in cases where a device (stent) is inserted in the blood vessel to keep it open.
Breast cancer – Consuming folate in the diet might lower the risk of developing breast cancer in women who also eat high amounts of methionine, vitamin B12 (cyanocobalamin), or vitamin B6 (pyridoxine), but research is not consistent. Other research suggests that taking folic acid supplements alone does not lower the risk of breast cancer.
Heart disease – Most research shows that taking folic acid alone or with other B vitamins does not reduce the risk of death or heart disease-related events in people with heart disease.
Cataracts – Research shows that taking folic acid with other vitamins including vitamin B6 and vitamin B12 does not prevent cataracts. In fact, it might increase the chance of needing to have cataracts removed.
Chronic fatigue syndrome – Daily injections of folic acid appear to have no effect on symptoms of chronic fatigue syndrome.
Diarrhea – Taking a specific nutritional supplement with added folic acid and possibly vitamin B12 does not seem to prevent diarrhea in children at risk of malnutrition. Taking this product may increase the risk of having diarrhea last more than a few days.
Preventing falls – Taking folic acid with vitamin B-12 does not seem to prevent falls in older people who are also taking vitamin D.
Fetal and early infant death – Taking folic acid during pregnancy does not seem to reduce the risk of having a baby die just before or after birth.
Toxicity from the drug lometrexol – Daily injections of folic acid appear to have no effect on symptoms of chronic fatigue syndrome.
Lower respiratory tract infections – Taking a specific nutritional supplement with added folic acid and possibly vitamin B12 does not seem to prevent infections in the lungs in children at risk of malnutrition.
Weak bones (osteoporosis) – In elderly individuals with osteoporosis, taking folic acid with vitamin B12 and possibly vitamin B6 (pyridoxine) does not seem to prevent broken bones.
Performance in older people – Taking folic acid with vitamin B-12 doesn’t seem to help older people walk better or have stronger hands.
Growths in the large intestine and rectum (colorectal adenoma) – Taking folic acid supplements does not seem to prevent growths in the large intestine or rectum.
Inherited disease called Fragile-X syndrome – Taking folic acid by mouth does not improve symptoms of fragile-X-syndrome.
Premature infants – Taking folic acid during pregnancy does not decrease the risk of having a premature baby.
Insufficient Evidence for
Acne – Limited evidence suggests that taking a specific nutritional supplement, containing vitamin B3 (nicotinamide), a compound isolated from grains (azelaic acid), zinc, vitamin B6 (pyridoxine), copper, and folic acid (NicAzel, Elorac Inc., Vernon Hills, IL) appears to reduce inflammation associated with pimples on the face.
Alzheimer’s disease – Limited evidence suggests that elderly people who consume more folic acid than the recommended dietary allowance (RDA) appear to have a lower risk of developing Alzheimer’s disease than people who consume less folic acid.
Autism – Limited research suggests taking folic acid during pregnancy might reduce the risk of autism in the child.
Beta-thalassemia – Beta-thalassemia is a disorder of the blood that results in the production of less hemoglobin, the protein that carries oxygen in the blood. Patients with beta-thalassemia usually have bone and muscle pain and have less strength. In children with this disorder, limited research suggests taking folic acid by itself, or with L-carnitine a compound similar to an amino acid from protein, might reduce bone pain and help increase strength.
Bipolar disorder – Taking folic acid does not appear to improve the antidepressant effects of lithium in people with bipolar disorder. However, taking folate with the medication valproate improves the effects of valproate.
Cervical cancer – There is some evidence that increasing folic acid and folate intake from dietary and supplement sources, along with thiamine, riboflavin, and vitamin B12, might help to prevent cervical cancer.
Long-term kidney disease (chronic kidney disease, CKD) – Taking folic acid might help slow kidney function decline in people with CKD. But it is not beneficial when used along with vitamin B12 (cyanocobalamin). In fact, the combination might make kidney disease worse.
Colon cancer, rectal cancer – Research suggests that taking folic acid or eating folate in the diet can reduce the risk of developing colon or rectal cancer. However, there is some research that does not suggest that taking folic acid or folate in the diet offers the same benefit. It is possible that folic acid may be more helpful for preventing colon cancer than rectal cancer or it may be more helpful for specific kinds of colon cancer.
Diabetes – Taking folic acid supplements does not seem to benefit people with diabetes.
Epilepsy – Taking folic acid does not reduce seizures in people with epilepsy.
Esophageal cancer – Research suggests that consuming more folate in the diet lowers the risk for developing esophageal cancer.
High amounts of homocysteine in the blood caused by the drug fenofibrat – Taking folic acid every other day might lower levels of homocysteine in the blood caused by the drug fenofibrate.
Stomach cancer – Research suggests that taking folic acid reduces the risk of developing some types of stomach cancer.
Gout – Early research suggests that folate might reduce the risk of gout.
Head and neck cancer – Getting more folic acid from the diet has been linked to a lower risk of head and neck cancer.
Hearing loss – Low levels of folate in the blood seem to be related to the risk for sudden hearing loss in adults. Some evidence suggests that taking folic acid daily for 3 years slows the decline of hearing loss in older people who have low folate levels. It is not clear if folic acid supplementation reduces hearing loss in people with normal folate levels.
Male infertility – Some research suggests that taking folic acid plus zinc sulfate daily can increase sperm count in men with low sperm counts.
Low birth weight – Taking folic acid during pregnancy does not prevent some babies from being born at a low birth weight but it does seem to increase the overall average of birth weights. However, some early research suggests that taking folic acid before getting pregnant might reduce the risk of having a baby that is too small even when born full term. Although this risk is not reduced in mothers that start supplementation after the baby is conceived.
Lung cancer – There does not appear to be a relationship between low levels of folic acid and lung cancer in most people.
A type of skin cancer called melanoma – Early research shows that taking folic acid might reduce the risk of melanoma.
Helping medicines used for chest pain work longer – Some evidence suggests that taking folic acid does not help medications for chest pain (nitrates) work longer.
Cleft lip – Some research suggests that taking folic acid during pregnancy lowers the risk of left lip. However, other research shows no effect.
Pancreatic cancer – Eating more than 280 mcg of folate in the diet daily is linked to a lower risk of developing pancreatic cancer. However, other research suggests that folate intake is not linked to pancreatic cancer risk.
Nerve pain (peripheral neuropathy) – There is conflicting evidence about the role of folic acid in nerve pain for people with diabetes (diabetic neuropathy). Some research suggests that taking folic acid with vitamin B6 (pyridoxine) and vitamin B12 improves some symptoms of nerve pain so that people feel happier. However, the nerves do not seem to function any better.
Cancer of the throat – Limited research suggests folic acid and folate from dietary and sources and supplements may protect against oropharyngeal cancer, a specific type of throat cancer.
Pre-eclampsia – Pre-eclampsia is marked by high blood pressure and protein in the urine during pregnancy. Limited research suggests taking folic acid supplements during pregnancy does not reduce the risk of pre-eclampsia.
Pregnancy-induced high blood pressure – Limited research suggests that taking folic acid during pregnancy does not reduce the risk of high blood pressure (gestational hypertension).
A disorder that causes a strong urge to move ones legs (restless legs syndrome; RLS) – Taking folic acid seems to reduce symptoms of restless legs syndrome. Researchers are studying whether folic acid deficiency causes restless legs syndrome.
Schizophrenia – Taking a combination of folic acid and vitamin B12 may reduce some of the negative symptoms associated with schizophrenia, but only in some patients with a specific genetic make-up. In most people, folic acid does not help with these symptoms.
Sickle-cell disease. Taking folic acid might lower homocysteine levels. However, it is not known if this will benefit people with sickle-cell disease.
Alcoholism
Liver disease
The European Food Safety Authority (EFSA), which provides scientific advice to assist policy makers, has confirmed that clear health benefits have been established for the dietary intake of folate (vitamin B9) in contributing to:
normal blood formation;
normal homocysteine;
a normal metabolism of the immune system;
normal cell division;
normal maternal tissue growth during pregnancy;
normal amino acid synthesis;
normal psychological functions;
the reduction of tiredness and fatigue;
maintanance of normal vision;
In addition, the EFSA has confirmed that supplemental folate intake increases maternal folate status, which contributes to the reduction of the risk of neural tube defects (NTD).
Puncture Wounds/Wounds are defined as a disruption of the normal structure and function of skin and underlying soft tissue that is caused by trauma or chronic mechanical stress (e.g., decubitus ulcers). Wounds can be broken down into acute or chronic, and open or closed. Wound treatment is performed according to pathology, the extent, and circumstances of the lesions. To heal, the wound needs to have a vascular supply, be free of necrotic tissue, clear of infection, and moist. General wound treatment includes surgical wound closure, open wound treatment, and plastic reconstruction of skin defects. In addition, infectious or concomitant disease prevention should be considered (e.g., antibiotic therapy, vaccines for tetanus and rabies, diabetes control).
A wound is damaged or disruption to the skin and, before treatment, the exact cause, location, and type of wound must be assessed to provide appropriate treatment.[rx][rx][rx] Each clinician will have widely differing and distinct opinions and understanding of wound care depending on their prior experience. The reason for this because of the widely differing and distinct types of wounds, each with their etiology. An ostomy nurse will have a completely different approach to wound care that will require an orthopedic surgeon who deals with trauma and both will be far different from a dermatologist who treats burn victims. Nevertheless, each of these healthcare providers is performing wound care. How do professionals then approach wound assessment when the causes are so diverse? Below are some basic questions to ask during a wound assessment to best classify and treat a wound presenting in a clinical setting.
Normal Healthy Skin of Wounds
As the interface between the environment and body, the skin has several distinct functions. It protects the underlying tissues from abrasions, the entry of microbes, unwanted water loss, and ultraviolet light damage. Tactile sensations of touch, pressure, and vibration, thermal sensations of heat and cold, and pain sensations all originate in the skin’s nervous system. The body’s thermoregulation relies on the skin’s ability to sweat and to control the flow of blood to the skin to increase or decrease heat loss. The skin’s functions are performed by three distinct tissue layers: a thin outer layer of cells called the epidermis, a thicker middle layer of connective tissue called the dermis, and an inner, subcutaneous layer. The outer layers of the epidermis are composed of flattened, cornified dead keratinocytes that form a barrier to water loss and microbe entry. These cells are derived from a basal layer of constantly dividing keratinocytes that lies next to the dermis. The epidermis does not contain nerves or blood vessels and obtains water and nutrients through diffusion from the dermis. The dermis is composed mostly of collagen fibers and some elastic fibers both produced by fibroblasts and, along with water and large proteoglycan molecules, makes up the extracellular matrix. This layer of the skin provides mechanical strength and a substrate for water and nutrient diffusion; it contains blood vessels, nerves, and cells involved in immune function, growth, and repair. The dermis also contains sweat glands, oil glands, and hair follicles. The subcutaneous layer is composed of adipocytes that form a thick layer of adipose tissue.[rx]
Types of Wounds
Each of the potential underlying causes must be addressed for the wound to heal. Before determining the underlying cause, it is important to determine what type of wound the patient has. These subclassifications can be acute or chronic.[rx][rx][rx]
1. According to the severity, a wound can be classified as
Acute
Clinicians assess acute wounds by the method of injury and damage to the soft tissues and bony structures. In crush or high impact injuries, there is an area of demarcation which is not fully recognized until sometimes as much as a week or 2 later. For this reason, it is important to determine the method of injury and to keep in mind that the wound seen is not necessarily the entirety of the wound which will be present in a week. In these cases, the patient and their family should be educated on this progression to prevent frustration and misunderstanding.
For all acute types of wounds, it is important to determine the length of time since injury (days or hours), the involvement of neurovascular supply, muscle, tendon, ligament, and bony involvement, and the likelihood of contaminants in the wound. Also of importance is when the patient had their last tetanus shot. CLinicians should start antibiotics if the wound is severely contaminated or if it is longer than 3 hours since the injury. All underlying tissue should be repaired if possible, and the wound should be irrigated to remove contaminants and bacteria.
In cases of open fracture the most used classification is Gustillo-Anderson
Type 1 – Clean wound, less than one cm with minimal soft tissue damage, adequate soft tissue coverage of bone, and no periosteal stripping
Type 2 – Wound with moderate contamination, greater than one cm with moderate soft tissue damage, adequate soft tissue coverage of bone, and no periosteal stripping
Type 3A – Wound with significant contamination, with significant soft tissue damage, adequate soft tissue coverage of bone, and periosteal stripping is present
Type 3B – Wound with significant contamination, with significant soft tissue damage, unable to cover bone with soft tissue (requiring graft), and periosteal stripping
Type 3C – Similar to type A or B, however with Arterial damage requiring repair
Chronic
If a wound becomes arrested in progression through the normal stages of inflammation and wound healing and remains open, then this becomes a chronic wound. While there is no consensus as to when a wound becomes chronic, a study by Sheehan et. al determined that in diabetic wounds, the degree of healing at 4 weeks is a strong predictor of 12 week healing, suggesting that those wounds which have not healed approximately 50% in 4 weeks are likely to have an arrested healing process, and therefore are chronic.[rx][rx]
In the chronic setting, the main goal is to identify why the wound is not healing and to fix this obstacle or obstacles.
There are a limited number of reasons a wound becomes chronic; however, once these reasons are rectified, the wound resumes its natural course of healing.
Arterial – Is there enough blood flow? Generally speaking, an ABI of less than 50 mm Hg, or an absolute toe pressure less than 30 mm Hg (or less than 50 mm Hg for persons with diabetes) indicates critical limb ischemia and predicts failure of wounds to heal.
Venous – Pressure-induced changes in blood vessel wall permeability then lead to leakage of fibrin and other plasma components into the perivascular space. Accumulation of fibrin has direct and negative effects on wound healing as it down-regulates collagen synthesis.
Infection – Underlying infectious processes including cellulitic and osteomyelitis processes will inhibit wound healing. Culturing for aerobic, anaerobic, and fungal pathogens is recommended.
Pressure – Increased pressure to the area of concern will destroy new tissue growth and prevent proper perfusion of blood to the wound site. These areas need to be offloaded to avoid pressure in the area.
Oncologic – Always biopsy areas of concern in nonhealing wounds, as this can be an atypical presentation of some types of malignancies.
Systemic – There are multiple systemic diseases which inhibit wound healing, with diabetes being the most common culprit. It has been determined that uncontrolled blood glucose levels suppresses the body’s normal inflammatory response, as well as causing microvascular disease which limits healing.
Nutrition – While serum albumin has not been found to be a good predictor of wound healing, there is some evidence that protein malnutrition, as well as insufficient levels of certain vitamins and minerals, will limit the body’s ability to heal chronic wounds.
Pharmacological – Hydroxyurea has been reported in multiple instances to cause nonhealing ulcerations.
Self-inflicted/psychosocial – There are instances where a patient is causing the ulceration, either on purpose or as a result of noncompliance. This is often the hardest factor to spot and overcome, but must always be a consideration.
2. According to level of contamination, a wound can be classified as
Clean wound – made under sterile conditions where there are no organisms present, and the skin is likely to heal without complications.
Contaminated wound – usually resulting from accidental injury; there are pathogenic organisms and foreign bodies in the wound.
Infected wound – the wound has pathogenic organisms present and multiplying, exhibiting clinical signs of infection (yellow appearance, soreness, redness, oozing pus).
Colonized wound – a chronic situation, containing pathogenic organisms, difficult to heal (i.e. bedsore).
Open
Open wounds can be classified according to the object that caused the wound
Incisions or incised wounds – caused by a clean, sharp-edged object such as a knife, razor, or glass splinter.
Lacerations – irregular tear-like wounds caused by some blunt trauma. Lacerations and incisions may appear linear (regular) or stellate (irregular). The term laceration is commonly misused in reference to incisions.[rx]
Abrasions (grazes) – superficial wounds in which the topmost layer of the skin (the epidermis) is scraped off. Abrasions are often caused by a sliding fall onto a rough surface such as asphalt, tree bark or concrete.
Avulsions – injuries in which a body structure is forcibly detached from its normal point of insertion. A type of amputation where the extremity is pulled off rather than cut off. When used in reference to skin avulsions, the term ‘degloving’ is also sometimes used as a synonym.
Puncture wounds – caused by an object puncturing the skin, such as a splinter, nail or needle.
Penetration wounds – caused by an object such as a knife entering and coming out from the skin.
Gunshot wounds – caused by a bullet or similar projectile driving into or through the body. There may be two wounds, one at the site of entry and one at the site of exit, generally referred to as a “through-and-through.”
Closed
Closed wounds have fewer categories, but are just as dangerous as open wounds:
Hematomas (or blood tumor) – caused by damage to a blood vessel that in turn causes blood to collect under the skin.
Hematomas that originate from internal blood vessel pathology are petechiae, purpura, and ecchymosis. The different classifications are based on size.
Hematomas that originate from an external source of trauma are contusions, also commonly called bruises.
Crush injury – caused by a great or extreme amount of force applied over a long period of time.
3. According to the Visuality, a wound can be classified as
Internal Wounds
Disturbance of the different regulating systems of the human body can lead to wound formation, and may include the following:
Impaired circulation – This can be from either ischemia or stasis. Ischemia is the result of reduced blood supply caused by the narrowing or blockage of blood vessels, which leads to poor circulation. Stasis is caused by immobilization (or difficulty moving) for long periods or failure of the regulating valves in the veins, which leads to blood pooling and failing to flow normally to the heart.
Neuropathy – This is seen mostly in cases of prolonged uncontrolled diabetes mellitus, where high blood sugars, derivative proteins and metabolites accumulate and damage the nervous system. The patients are usually unaware of any trauma or wounds, mainly due to loss of sensation in the affected area.
Medical illness – When chronic and uncontrolled for long periods (such as hypertension, hyperlipidemia, arthrosclerosis, diabetes mellitus, AIDS, malignancy, morbid obesity, hepatitis C virus, etc.), medical illnesses can lead to impairment of the immune system functions, diminishing the circulation and damaging other organs and systems.
External Wounds
External wounds can either be open or closed. In cases of closed wounds, the skin is intact and the underlying tissue is affected but not directly exposed to the outside environment. The following are the most common types of closed wounds:
Contusions – These are a common type of sports injury, where a direct blunt trauma can damage the small blood vessels and capillaries, muscles and underlying tissue, as well the internal organs or bone. Contusions present as a painful bruise with reddish to bluish discoloration that spreads over the injured area of skin.
Hematomas – These include any injury that damages the small blood vessels and capillaries resulting in blood collecting and pooling in a limited space. Hematomas typically present as a painful, spongy rubbery lump-like lesion. Depending on the severity and site of the trauama, hematomas can be small or large, deep inside the body or just under the skin.
Crush injuries – These are usually caused by an external high-pressure force that squeezes part of the body between two surfaces. The degree of injury can range from a minor bruise to a complete destruction of the crushed area of the body, depending on the site, size, duration and power of the trauma.
Causes of Wound
Sudden forceful fall down
Road traffic accident
Burn and injured suddenly
Falls – Falling onto an outstretched hand is one of the most common causes of wound.
Sports injuries – Many sports injury occur during contact sports or sports in which you might fall onto an outstretched hand — such as in-line skating or snowboarding.
Motor vehicle crashes – Motor vehicle crashes can cause wound. Sometimes into many pieces, and often require surgical repair.
Have osteoporosis – a disease that weakens your bones.
Eave low muscle mass or poor muscle strength – or lack agility and have poor balance (these conditions make you more likely to fall)
Walk or do other activities in snow or on the ice – or do activities that require a lot of forwarding momenta, such as in-line skating and skiing
Wave an inadequate intake of calcium or vitamin D
Football or soccer, especially on artificial turf
Rugby
Horseback riding
Hockey
Skiing
Snowboarding
In-line skating
Jumping on a trampoline
Symptoms of Wound
General signs and symptoms of a wound infection include
Increased firmness of skin or swelling around the wound bed
Increasing drainage from the wound bed
Delayed wound healing
Discoloration of the wound bed with it turning darker in color
Foul odor
Increased fragility of the wound bed
Wound breakdown /enlargement
The skin may harden or tighten in the area and red streaks may radiate from the wound. Wound infections may also cause fevers, especially when they spread to the blood.
Diagnosis of Wound
Clinicians perform wound assessment as a means for determining the appropriate treatment for an extremely diverse grouping of disease processes. Just as hypertension is not treated the same as diabetes, each of the underlying etiologies of the given wound must be identified and treated as if it were its own disease, not a blanket classification of “wound.”[rx][rx]
The initial assessment should begin with the following:
How – How was the wound created and, if chronic, why is it still open? (underlying etiology)
Where – Where on the body is it located? Is it in an area which is difficult to offload, or to keep clean? Is it in an area of high skin tension? Is it near any vital structures such as a major artery?
When – How long has this wound been present? (eg., chronic or acute)
What – What anatomy does it extend? (e.g., epidermis, dermis, subcutaneous tissue, fascia, muscle, tendon, bone, arteries, nerves)
What – What co-morbidities or social factors does the patient have which might affect which might affect their ability to heal the wound?
Is it life threatening?
All of these factors significantly affect the treatment plan moving forward. While there are many excellent biologics, skin grafts, and other options available, without the appropriate understanding of the nature of the wound the chances of healing decline significantly.
Issues of Concern
While some wounds are simple, the majority of wounds many clinicians encounter are caused by or complicated by some other issue.[rx][rx][rx][rx] These are a few of the possible complications from different wound types:
A chronic wound will have a different makeup than that of an acute wound, requiring conversion for healing.
An underlying infection will prevent wound healing even if the infection is subacute.
A damaged or constricted arterial supply will prevent appropriate blood flow to the wound.
A damaged venous supply will cause venous stasis.
Physical pressure on chronic ulceration will cause repeated damage, preventing healing.
Tests
Many minor and superficial skin and wound infections are diagnosed by a healthcare practitioner based on a physical examination, sign and symptoms, and experience. A clinical evaluation cannot, however, definitively tell the healthcare practitioner which microbe is causing a wound infection or what treatment is likely to be effective. For that, laboratory testing is required.
Laboratory Tests
Examples of common tests include
Bacterial culture – This is the primary test used to diagnose a bacterial infection. Results are usually available within 24-48 hours.
Gram stain – This is usually performed in conjunction with the wound culture. It is a special staining procedure that allows bacteria to be evaluated under the microscope. The results are usually available the same day and provide preliminary information about the microbe that may be causing the infection.
Antimicrobial susceptibility – A follow-up test to a positive wound culture, this is used to determine the bacteria’s likely susceptibility to certain drugs and helps the healthcare practitioner select appropriate antibiotics for treatment. Results are typically available in about 24 hours. This testing can identify resistant bacteria such as MRSA.
Other tests may include
KOH prep – This is a rapid test performed to detect fungi in a sample. The sample is treated with a special solution, placed on a slide, and examined under a microscope.
Fungal culture – This is ordered when a fungal infection is suspected. Many fungi are slow-growing and may take several weeks to identify.
AFB testing – This is ordered when a mycobacterial infection is suspected. Most AFB are slow-growing and may take several weeks to identify.
Blood culture – This is ordered when infection from a wound may have spread to the blood.
Molecular testing – to detect genetic material of a specific microbe
Basic metabolic panel (BMP) or Comprehensive metabolic panel (CMP) – This may be ordered to detect underlying conditions that can affect wound healing, such as a glucose test to detect diabetes.
Complete blood count (CBC) – An elevated white blood cell (WBC) count may be a sign of infection.
Treatment of Wound
Emergency Management
Pain control
Intravenous opiates are often used as patients typically in severe pain
Highly effective for management of pain
Lower side effect profile than systemic analgesia
Always calculate your toxic dose of local anesthetic to avoid local anesthetic systemic toxicity
Closed the wounds should be placed in long leg splint and can also be placed in traction
If open Fractures should receive antibiotics and should proceed to OR for irrigation/debridement.
Cleaning to remove dirt and debris from a fresh wound. This is done very gently and often in the shower.
Vaccinating for tetanus may be recommended in some cases of traumatic injury.
Exploring a deep wound surgically may be necessary. Local anaesthetic will be given before the examination.
Removing dead skin surgically. Local anaesthetic will be given.
Closing large wounds with stitches or staples.
Dressing the wound – The dressing chosen by your doctor depends on the type and severity of the wound. In most cases of chronic wounds, the doctor will recommend a moist dressing.
Relieving pain with medications – Pain can cause the blood vessels to constrict, which slows healing. If your wound is causing discomfort, tell your doctor. The doctor may suggest that you take over-the-counter drugs such as paracetamol or may prescribe stronger pain-killing medication.
Treating signs of infection including pain – pus and fever. The doctor will prescribe antibiotics and antimicrobial dressings if necessary. Take as directed.
Skin Traction (Hare or Thomas) if needed
May improve wound alignment, blood flow, and pain
Skin traction splint can cause complications if a patient with a significant injury (i.e. multi ligamentous knee injury)
Here we review only the commonly used medications that have a significant impact on healing, including glucocorticoid steroids, non-steroidal anti-inflammatory drugs, and chemotherapeutic drugs.
Glucocorticoid Steroids – Systemic glucocorticoids (GC), which are frequently used as anti-inflammatory agents, are well-known to inhibit wound repair via global anti-inflammatory effects and suppression of cellular wound responses, including fibroblast proliferation and collagen synthesis. Systemic steroids cause wounds to heal with incomplete granulation tissue and reduced wound contraction [rx]. Glucocorticoids also inhibit production of hypoxia-inducible factor-1 (HIF-1), a key transcriptional factor in healing wounds [rx].
Non-steroidal Anti-inflammatory Drugs – Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen are widely used for the treatment of inflammation and rheumatoid arthritis and for pain management. Low-dosage aspirin, due to its anti-platelet function, is commonly used as a preventive therapeutic for cardiovascular disease, but not as an anti-inflammatory drug [rx]. There are few data to suggest that short-term NSAIDs have a negative impact on healing.
Opioids – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.
Calcium & vitamin D3 – To improve bones health and healing fracture. As a general rule, men and women age 50 and older should consume 1,200 milligrams of calcium a day, and 600 international units of vitamin D a day.
Glucosamine & Diacerein, Chondroitin sulfate – can be used to tightening the loose tendon, cartilage, ligament, and cartilage, ligament regenerates cartilage or inhabits the further degeneration of cartilage, ligament.
Chemotherapeutic Drugs – Most chemotherapeutic drugs are designed to inhibit cellular metabolism, rapid cell division, and angiogenesis and thus inhibit many of the pathways that are critical to appropriate wound repair. These medications inhibit DNA, RNA, or protein synthesis, resulting in decreased fibroplasia and neovascularization of wounds [rx].
Nutrition – For more than 100 years, nutrition has been recognized as a very important factor that affects wound healing. Most obvious is that malnutrition or specific nutrient deficiencies can have a profound impact on wound healing after trauma and surgery. Patients with chronic or non-healing wounds and experiencing nutrition deficiency often require special nutrients. Energy, carbohydrate, protein, fat, vitamin, and mineral metabolism all can affect the healing process [rx].
Carbohydrates, Protein, and Amino Acids – Together with fats, carbohydrates are the primary source of energy in the wound-healing process. Glucose is the major source of fuel used to create the cellular ATP that provides energy for angiogenesis and deposition of the new tissues [rx]. The use of glucose as a source for ATP synthesis is essential in preventing the depletion of other amino acid and protein substrates [rx].
Protein – is one of the most important nutrient factors affecting wound healing. A deficiency of protein can impair capillary formation, fibroblast proliferation, proteoglycan synthesis, collagen synthesis, and wound remodeling. A deficiency of protein also affects the immune system, with resultant decreased leukocyte phagocytosis and increased susceptibility to infection [rx]. Collagen is the major protein component of connective tissue and is composed primarily of glycine, proline, and hydroxyproline. Collagen synthesis requires hydroxylation of lysine and proline, and co-factors such as ferrous iron and vitamin C. Impaired wound healing results from deficiencies in any of these co-factors [rx].
Arginine – is a semi-essential amino acid that is required during periods of maximal growth, severe stress, and injury. Arginine has many effects in the body, including modulation of immune function, wound healing, hormone secretion, vascular tone, and endothelial function. Arginine is also a precursor to proline, and, as such, sufficient arginine levels are needed to support collagen deposition, angiogenesis, and wound contraction [rx][rx]. Arginine improves immune function, and stimulates wound healing in healthy and ill individuals [rx]. Under psychological stress situations, the metabolic demand of arginine increases, and its supplementation has been shown to be an effective adjuvant therapy in wound healing [rx].
Glutamine – is the most abundant amino acid in plasma and is a major source of metabolic energy for rapidly proliferating cells such as fibroblasts, lymphocytes, epithelial cells, and macrophages [rx]. The serum concentration of glutamine is reduced after major surgery, trauma, and sepsis, and supplementation of this amino acid improves nitrogen balance and diminishes immunosuppression [rx]. Glutamine has a crucial role in stimulating the inflammatory immune response occurring early in wound healing [rx]. Oral glutamine supplementation has been shown to improve wound breaking strength and to increase levels of mature collagen [rx].
Fatty Acids – Lipids are used as nutritional support for surgical or critically ill patients to help meet energy demands and provide essential building blocks for wound healing and tissue repair. Polyunsaturated fatty acids (PUFAs), which cannot be synthesized de novo by mammals, consist mainly of two families, n-6 (omega-6, found in soybean oil) and n-3 (omega-3, found in fish oil). Fish oil has been widely touted for the health benefits of omega-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The effects of omega-3 fatty acids on wound healing are not conclusive. They have been reported to affect pro-inflammatory cytokine production, cell metabolism, gene expression, and angiogenesis in wound sites [rx] . The true benefit of omega-3 fatty acids may be in their ability to improve the systemic immune function of the host, thus reducing infectious complications and improving survival [rx].
Vitamins, Micronutrients, and Trace Elements – Vitamins C (L-ascorbic acid), A (retinol), and E (tocopherol) show potent anti-oxidant and anti-inflammatory effects. Vitamin C has many roles in wound healing, and a deficiency in this vitamin has multiple effects on tissue repair. Vitamin C deficiencies result in impaired healing, and have been linked to decreased collagen synthesis and fibroblast proliferation, decreased angiogenesis, and increased capillary fragility. Also, vitamin C deficiency leads to an impaired immune response and increased susceptibility to wound infection [rx;rx]. Similarly, vitamin A deficiency leads to impaired wound healing. The biological properties of vitamin A include anti-oxidant activity, increased fibroblast proliferation, modulation of cellular differentiation and proliferation, increased collagen and hyaluronate synthesis, and decreased MMP-mediated extracellular matrix degradation [rx].
Vitamin E, an anti-oxidant – maintains and stabilizes cellular membrane integrity by providing protection against destruction by oxidation. Vitamin E also has anti-inflammatory properties and has been suggested to have a role in decreasing excess scar formation in chronic wounds. Animal experiments have indicated that vitamin E supplementation is beneficial to wound healing [rx, rx; rx] and topical vitamin E has been widely promoted as an anti-scarring agent. However, clinical studies have not yet proved a role for topical vitamin E treatment in improving healing outcomes [rx,rx].
Several micronutrients – have been shown to be important for optimal repair. Magnesium functions as a co-factor for many enzymes involved in protein and collagen synthesis, while copper is a required co-factor for cytochrome oxidase, for cytosolic anti-oxidant superoxide dismutase, and for the optimal cross-linking of collagen. Zinc is a co-factor for both RNA and DNA polymerase, and a zinc deficiency causes a significant impairment in wound healing. Iron is required for the hydroxylation of proline and lysine, and, as a result, severe iron deficiency can result in impaired collagen production [rx,rx;rx, rx; rx].
Normal Wound-healing Process
Phase
Cellular and Bio-physiologic Events
Hemostasis
vascular constriction
platelet aggregation, degranulation, and fibrin formation (thrombus)
Inflammation
neutrophil infiltration
monocyte infiltration and differentiation to macrophage
lymphocyte infiltration
Proliferation
re-epithelialization
angiogenesis
collagen synthesis
ECM formation
Remodeling
collagen remodeling
vascular maturation and regression
Dressing
Some of the unique features of each are described below.
The following dressings may be used on chronic or acute wounds depending on the nature of the wound.
Low or nonadherent dressings – are inexpensive and allow wound exudate to pass through into a secondary dressing while helping to maintain a moist wound environment. These dressings are specially designed to reduce adherence to the wound bed. Non adherent dressings are made from open weave cloth soaked in paraffin, textiles, or multilayered or perforated plastic films. This type of dressing is suitable for flat, shallow wounds with low exudate such as a venous leg ulcer.
Hydrocolloid dressings – are composed of adhesive, absorbent, and elastomeric components. Carboxymethylcellulose is the most common absorptive ingredient. They are permeable to moisture vapor, but not to water. Additionally, they facilitate autolytic débridement, are self-adhesive, mold well, provide light-to-moderate exudate absorption, and can be left in place for several days, minimizing skin trauma and disruption of the healing process. They are intended for use on light-to-moderate exuding, acute or chronic partial- or full-thickness wounds but are not intended for use on infected wounds. Upon sustained contact with wound fluid, the hydrocolloid forms a gel.
Foam dressings – vary widely in composition and construction. They consist of a polymer, often polyurethane, with small, open cells that are able to hold fluids. Some varieties of foam dressings have a waterproof film covering the top surface and may or may not have an adhesive coating on the wound contact side or border. Foams are permeable to water and gas, and are able to absorb light to heavy exudate. This type of dressing is frequently used under compression stockings in patients with venous leg ulcers.
Film dressings consist of a single – thin transparent sheet of polyurethane coated on one side with an adhesive. The sheet is permeable to gases and water vapor but impermeable to wound fluids. Film dressings retain moisture, are impermeable to bacteria and other contaminants, allow wound observation, and do not require a secondary dressing. Excessive fluid buildup may break the adhesive seal and allow leakage. Film dressings are intended for superficial wounds with little exudate and are commonly used as a secondary dressing to attach a primary absorbent dressing. The dressing may remain in place for up to seven days if excessive fluid does not accumulate. Film dressings have been used extensively to treat split-thickness graft donor sites.
Alginate dressings – are made from calcium or calcium-sodium salts of natural polysaccharides derived from brown seaweed. When the alginate material comes into contact with sodium-rich wound exudates, an ion exchange takes place and produces a hydrophilic gel. This hydrophilic gel is capable of absorbing up to 20 times its weight and does not adhere to the wound. This dressing can remain in place for about seven days if enough exudate is present to prevent drying. This category of dressing is best suited for moist, moderate-to-heavy exuding wounds. Alginate dressings require a secondary dressing, such as a film dressing, to hold them in place and to prevent the alginate from drying out.
Hydrofiber dressing – is composed of sodium carboxymethylcellulose fibers.[rx] The fibers maintain a moist wound environment by absorbing large amounts of exudate and forming a gel. This dressing is not intended for lightly exuding wounds. A secondary dressing is required.
Hydrogel sheets – are three-dimensional networks of cross-linked hydrophilic polymers. Their high water content provides moisture to the wound, but these dressings can absorb small-to-large amounts of fluid, depending on their composition. Depending on wound exudate levels, hydrogels may require more frequent dressing changes, every 1–3 days, compared with other synthetic dressings. Hydrogel sheets can be used on most wound types but may not be effective on heavily exuding wounds. The gel may also contain additional ingredients such as collagens, alginate, or complex carbohydrates. Amorphous hydrogels can donate moisture to a dry wound with eschar and facilitate autolytic débridement in necrotic wounds. A second dressing may be used to retain the gel in shallow wounds.
Polymer-based dressing – Transforming methacrylate (TMD) was compared to carboxymethylcellulose (CMC-Ag) in one study of 34 patients. The study showed that TMD, compared to CMC-Ag, was associated with lower pain scores and better patient satisfaction, but the two dressings did not differ in terms of number of dressing changes and the time to complete healing.[rx] Suprathel (a polymer-based dressing) was evaluated in a study of 72 patients, and it was compared to a polyurethane dressings (Biatain-Ibu) and a silicone dressing (Mepitel). The three dressings had similar time to re-epithelialization, but Suprathel had a significantly lower number of dressing changes compared to the two other dressings.[rx]
Crystalline cellulose dressings – Results for the comparison between CMC-Ag and TMD are presented above.[rx] Veloderm was compared to Vaseline gauze in 96 patients.[rx] The study showed that Veloderm was associated with lower time to complete healing and number of dressing changes. The two dressings did not differ in terms of incidence of exudate, peri-lesional erythema or pain intensity.[rx]Rayon dressing was compared to Veloderm in a study of 14 patients and 28 skin graft donor sites.[rx] Rayon dressing showed lower dressing adherence to wound and lower 1st day pain score; the two dressings did not differ in terms of pain beyond day 14, hyperemia, edema and pruritus.[rx]
Alginate dressings – The study evaluated the dressing materials in terms of time to healing, pain scores, clinical infections and hypergranulation. Results showed that the six types of dressings did not differ with statistical significance except in the following cases: first, the semi-permeable films (Tegaderm or Opsite) were associated with lower pain scores than any other dressing type; second, the hydrocolloid dressing (DuoDerm E) required lower time (seven days difference) to healing than all other dressings; finally, the gauze dressings (Adaptic or Jelonet) were associated with the highest incidence of clinical infections.[rx]
Alginate-based dressings – were also evaluated in three other trials; the first one compared Algisite to a keratin dressing (Keramatrix).[rx]The trial showed that Algisite was associated with higher rate of epithelialization seven days after the operation than Keramatrix in patients older than 50 years; for younger patients, the rate of epithelialization did not significantly differ.[rx] Ding et al. compared time to healing and pain scores between alginate-silver dressing and hydrofiber dressing (Aquacel-A) in 10 patients and 20 donor sites; the results showed that the alginate dressing was associated with shorter time to healing and lower pain scores.[rx]The third trial compared Algisite covered by a polyurethane dressing (Opsite) to paraffin gauze dressing; the results showed that the two dressings did not differ in terms of pain scores, time to epithelialization and the assessment of general comfort. Algisite dressings required more dressing changes (34 times) than the paraffin gauze (4 times).[rx]
Polyurethane dressings – Opsite and Tegaderm films were evaluated in Brolemann’s study, and the results were presented above. Another trial compared the Opsite dressing to a hydrofiber dressing (Aquacel-A); the results showed that Opsite was associated with lower scores of pain.[rx] The Biatain-Ibu dressing was compared to Suprathel (polymer dressing) and Mepitel (silicone dressing); the results were presented above with polymer-based dressings.[rx] Another study compared Biatain-Ibu to a gauze dressing (Jelonet), and it was reported that Biatain-Ibu was associated with lower pain and itching than Jelonet; however, the study did not report any statistical testing for the differences between interventions.[rx]
Gauze dressings – Gauze dressings were evaluated in seven trials; the results of four trials were reported earlier in this section,[rx,rx,rx,rx]and the remaining three trials were as follows one trial compared Xeroform (gauze dressing) to a multilayer dressing and showed that Xeroform was associated with longer healing time and higher pain scores than Oxyband.[rx]The second trial compared paraffin gauze to a hydrofiber dressing (Aquacel) and reported that the paraffin gauze was associated with longer re-epithelialization time and higher pain score during dressing.[rx]The last trial compared Jelonet to a multilayer dressing as a dressing over a skin graft (receiver site); the results showed that the two dressings did not affect the time to graft take, number of nursing interventions, or post-operative infections; however, they showed that Jelonet was associated with higher pain score at the time of dressing removal.[rx]
Hydrocolloid dressings – The efficacy of DuoDerm E was compared to six other dressing materials in Brolmann’s trial; the results of this trial were presented earlier in this section.[rx]In another trial, DuoDerm was compared to a silicone-based dressing (AWBAT-D); the trial showed that the two dressings did not differ in terms of pain scores, wound size or time to discharge, but the DuoDerm was associated with shorter time to re-epithelialization.[rx]
Hydrofiber dressings – The efficacy of Aquacel was studied in six trials; the results of four trials were presented earlier in the section.[rx,rx,rx,rx]One of the remaining trials compared Aquacel to carbohydrate wound dressing (Glucan II), and it showed that the two interventions did not differ in terms of time to re-epithelialization, pain scores, or donor site infection.[rx]The second trial compared two different protocols of using Aquacel; in the first protocol, Aquacel dressing was covered with gauze, while in the second one, it was covered with polyurethane film (OpSite).[rx] The trial reported that the second protocol was associated with a larger number of donor sites healing at day 14 after surgery (88% versus 67%), and it was associated with lower pain during mobility the first day after operation; the two dressings did not differ in pain scores during rest at all time-point evaluations.[rx]
Silicone dressings – Four trials evaluated the efficacy of silicone-based dressings; the result three of trials were presented earlier in this section.[rx,rx,rx] The fourth trial compared Mepitel dressing to a nylon dressing (Bridal veil) when used over a skin graft (receiver site).[rx] The results of this trial showed that Mepitel dressing was associated with less pain, easier use, and better overall experience for patients.[rx]
Keratin dressings – The efficacy of Keranatrix was evaluated in one study the results of which were presented earlier in this section.[rx]
Self-adhesive fabric dressing (Mefix) with or without fibrin sealant – One trial evaluated the difference between using Mefix alone or with a fibrin sealant; the trial showed that the use of fibrin sealant was associated with lower daily pain and incapacity scores, but it did not affect the time to dressing removal or the time to discharge for the hospital.[rx]
Multilayer (combination) dressings – The efficacy of Oxyband and Allyven was evaluated in two studies the results of which were presented earlier in this section.[rx,rx]
Nylon dressings – The efficacy of Bridal veil was evaluated in one study the results of which were presented earlier in this section.[rx]
Carbohydrate wound dressings – The efficacy of Glucan dressing was evaluated in one study the results of which were presented earlier in this section.[rx]
Negative pressure dressings – One trial compared negative pressure dressings with a conventional dressing with gauze; both dressings were used over skin grafts (receiver sites).[rx]The trial reported that the negative pressure dressing was associated with a higher percentage of graft take and shorter duration of dressing.[rx]
Complication of Wound Healing
Factors that can slow the wound healing process include
Dead skin (necrosis) – dead skin and foreign materials interfere with the healing process.
Infection – an open wound may develop a bacterial infection. The body fights the infection rather than healing the wound.
Haemorrhage – persistent bleeding will keep the wound margins apart.
Mechanical damage – for example, a person who is immobile is at risk of bedsores because of constant pressure and friction.
Diet – poor food choices may deprive the body of the nutrients it needs to heal the wound, such as vitamin C, zinc and protein.
Medical conditions – such as diabetes, anaemia and some vascular diseases that restrict blood flow to the area, or any disorder that hinders the immune system.
Age – wounds tend to take longer to heal in elderly people.
Medicines – certain drugs or treatments used in the management of some medical conditions may interfere with the body’s healing process.
Smoking – cigarette smoking impairs healing and increases the risk of complications.
Varicose veins – restricted blood flow and swelling can lead to skin break down and persistent ulceration.
Dryness – wounds (such as leg ulcers) that are exposed to the air are less likely to heal. The various cells involved in healing, such as skin cells and immune cells, need a moist environment.
Abrasions Wound/Wounds are defined as a disruption of the normal structure and function of skin and underlying soft tissue that is caused by trauma or chronic mechanical stress (e.g., decubitus ulcers). Wounds can be broken down into acute or chronic, and open or closed. Wound treatment is performed according to pathology, the extent, and circumstances of the lesions. To heal, the wound needs to have a vascular supply, be free of necrotic tissue, clear of infection, and moist. General wound treatment includes surgical wound closure, open wound treatment, and plastic reconstruction of skin defects. In addition, infectious or concomitant disease prevention should be considered (e.g., antibiotic therapy, vaccines for tetanus and rabies, diabetes control).
A wound is damaged or disruption to the skin and, before treatment, the exact cause, location, and type of wound must be assessed to provide appropriate treatment.[rx][rx][rx] Each clinician will have widely differing and distinct opinions and understanding of wound care depending on their prior experience. The reason for this because of the widely differing and distinct types of wounds, each with their etiology. An ostomy nurse will have a completely different approach to wound care that will require an orthopedic surgeon who deals with trauma and both will be far different from a dermatologist who treats burn victims. Nevertheless, each of these healthcare providers is performing wound care. How do professionals then approach wound assessment when the causes are so diverse? Below are some basic questions to ask during a wound assessment to best classify and treat a wound presenting in a clinical setting.
Normal Healthy Skin of Wounds
As the interface between the environment and body, the skin has several distinct functions. It protects the underlying tissues from abrasions, the entry of microbes, unwanted water loss, and ultraviolet light damage. Tactile sensations of touch, pressure, and vibration, thermal sensations of heat and cold, and pain sensations all originate in the skin’s nervous system. The body’s thermoregulation relies on the skin’s ability to sweat and to control the flow of blood to the skin to increase or decrease heat loss. The skin’s functions are performed by three distinct tissue layers: a thin outer layer of cells called the epidermis, a thicker middle layer of connective tissue called the dermis, and an inner, subcutaneous layer. The outer layers of the epidermis are composed of flattened, cornified dead keratinocytes that form a barrier to water loss and microbe entry. These cells are derived from a basal layer of constantly dividing keratinocytes that lies next to the dermis. The epidermis does not contain nerves or blood vessels and obtains water and nutrients through diffusion from the dermis. The dermis is composed mostly of collagen fibers and some elastic fibers both produced by fibroblasts and, along with water and large proteoglycan molecules, makes up the extracellular matrix. This layer of the skin provides mechanical strength and a substrate for water and nutrient diffusion; it contains blood vessels, nerves, and cells involved in immune function, growth, and repair. The dermis also contains sweat glands, oil glands, and hair follicles. The subcutaneous layer is composed of adipocytes that form a thick layer of adipose tissue.[rx]
Types of Wounds
Each of the potential underlying causes must be addressed for the wound to heal. Before determining the underlying cause, it is important to determine what type of wound the patient has. These subclassifications can be acute or chronic.[rx][rx][rx]
1. According to the severity, a wound can be classified as
Acute
Clinicians assess acute wounds by the method of injury and damage to the soft tissues and bony structures. In crush or high impact injuries, there is an area of demarcation which is not fully recognized until sometimes as much as a week or 2 later. For this reason, it is important to determine the method of injury and to keep in mind that the wound seen is not necessarily the entirety of the wound which will be present in a week. In these cases, the patient and their family should be educated on this progression to prevent frustration and misunderstanding.
For all acute types of wounds, it is important to determine the length of time since injury (days or hours), the involvement of neurovascular supply, muscle, tendon, ligament, and bony involvement, and the likelihood of contaminants in the wound. Also of importance is when the patient had their last tetanus shot. CLinicians should start antibiotics if the wound is severely contaminated or if it is longer than 3 hours since the injury. All underlying tissue should be repaired if possible, and the wound should be irrigated to remove contaminants and bacteria.
In cases of open fracture the most used classification is Gustillo-Anderson
Type 1 – Clean wound, less than one cm with minimal soft tissue damage, adequate soft tissue coverage of bone, and no periosteal stripping
Type 2 – Wound with moderate contamination, greater than one cm with moderate soft tissue damage, adequate soft tissue coverage of bone, and no periosteal stripping
Type 3A – Wound with significant contamination, with significant soft tissue damage, adequate soft tissue coverage of bone, and periosteal stripping is present
Type 3B – Wound with significant contamination, with significant soft tissue damage, unable to cover bone with soft tissue (requiring graft), and periosteal stripping
Type 3C – Similar to type A or B, however with Arterial damage requiring repair
Chronic
If a wound becomes arrested in progression through the normal stages of inflammation and wound healing and remains open, then this becomes a chronic wound. While there is no consensus as to when a wound becomes chronic, a study by Sheehan et. al determined that in diabetic wounds, the degree of healing at 4 weeks is a strong predictor of 12 week healing, suggesting that those wounds which have not healed approximately 50% in 4 weeks are likely to have an arrested healing process, and therefore are chronic.[rx][rx]
In the chronic setting, the main goal is to identify why the wound is not healing and to fix this obstacle or obstacles.
There are a limited number of reasons a wound becomes chronic; however, once these reasons are rectified, the wound resumes its natural course of healing.
Arterial – Is there enough blood flow? Generally speaking, an ABI of less than 50 mm Hg, or an absolute toe pressure less than 30 mm Hg (or less than 50 mm Hg for persons with diabetes) indicates critical limb ischemia and predicts failure of wounds to heal.
Venous – Pressure-induced changes in blood vessel wall permeability then lead to leakage of fibrin and other plasma components into the perivascular space. Accumulation of fibrin has direct and negative effects on wound healing as it down-regulates collagen synthesis.
Infection – Underlying infectious processes including cellulitic and osteomyelitis processes will inhibit wound healing. Culturing for aerobic, anaerobic, and fungal pathogens is recommended.
Pressure – Increased pressure to the area of concern will destroy new tissue growth and prevent proper perfusion of blood to the wound site. These areas need to be offloaded to avoid pressure in the area.
Oncologic – Always biopsy areas of concern in nonhealing wounds, as this can be an atypical presentation of some types of malignancies.
Systemic – There are multiple systemic diseases which inhibit wound healing, with diabetes being the most common culprit. It has been determined that uncontrolled blood glucose levels suppresses the body’s normal inflammatory response, as well as causing microvascular disease which limits healing.
Nutrition – While serum albumin has not been found to be a good predictor of wound healing, there is some evidence that protein malnutrition, as well as insufficient levels of certain vitamins and minerals, will limit the body’s ability to heal chronic wounds.
Pharmacological – Hydroxyurea has been reported in multiple instances to cause nonhealing ulcerations.
Self-inflicted/psychosocial – There are instances where a patient is causing the ulceration, either on purpose or as a result of noncompliance. This is often the hardest factor to spot and overcome, but must always be a consideration.
2. According to level of contamination, a wound can be classified as
Clean wound – made under sterile conditions where there are no organisms present, and the skin is likely to heal without complications.
Contaminated wound – usually resulting from accidental injury; there are pathogenic organisms and foreign bodies in the wound.
Infected wound – the wound has pathogenic organisms present and multiplying, exhibiting clinical signs of infection (yellow appearance, soreness, redness, oozing pus).
Colonized wound – a chronic situation, containing pathogenic organisms, difficult to heal (i.e. bedsore).
Open
Open wounds can be classified according to the object that caused the wound
Incisions or incised wounds – caused by a clean, sharp-edged object such as a knife, razor, or glass splinter.
Lacerations – irregular tear-like wounds caused by some blunt trauma. Lacerations and incisions may appear linear (regular) or stellate (irregular). The term laceration is commonly misused in reference to incisions.[rx]
Abrasions (grazes) – superficial wounds in which the topmost layer of the skin (the epidermis) is scraped off. Abrasions are often caused by a sliding fall onto a rough surface such as asphalt, tree bark or concrete.
Avulsions – injuries in which a body structure is forcibly detached from its normal point of insertion. A type of amputation where the extremity is pulled off rather than cut off. When used in reference to skin avulsions, the term ‘degloving’ is also sometimes used as a synonym.
Puncture wounds – caused by an object puncturing the skin, such as a splinter, nail or needle.
Penetration wounds – caused by an object such as a knife entering and coming out from the skin.
Gunshot wounds – caused by a bullet or similar projectile driving into or through the body. There may be two wounds, one at the site of entry and one at the site of exit, generally referred to as a “through-and-through.”
Closed
Closed wounds have fewer categories, but are just as dangerous as open wounds:
Hematomas (or blood tumor) – caused by damage to a blood vessel that in turn causes blood to collect under the skin.
Hematomas that originate from internal blood vessel pathology are petechiae, purpura, and ecchymosis. The different classifications are based on size.
Hematomas that originate from an external source of trauma are contusions, also commonly called bruises.
Crush injury – caused by a great or extreme amount of force applied over a long period of time.
3. According to the Visuality, a wound can be classified as
Internal Wounds
Disturbance of the different regulating systems of the human body can lead to wound formation, and may include the following:
Impaired circulation – This can be from either ischemia or stasis. Ischemia is the result of reduced blood supply caused by the narrowing or blockage of blood vessels, which leads to poor circulation. Stasis is caused by immobilization (or difficulty moving) for long periods or failure of the regulating valves in the veins, which leads to blood pooling and failing to flow normally to the heart.
Neuropathy – This is seen mostly in cases of prolonged uncontrolled diabetes mellitus, where high blood sugars, derivative proteins and metabolites accumulate and damage the nervous system. The patients are usually unaware of any trauma or wounds, mainly due to loss of sensation in the affected area.
Medical illness – When chronic and uncontrolled for long periods (such as hypertension, hyperlipidemia, arthrosclerosis, diabetes mellitus, AIDS, malignancy, morbid obesity, hepatitis C virus, etc.), medical illnesses can lead to impairment of the immune system functions, diminishing the circulation and damaging other organs and systems.
External Wounds
External wounds can either be open or closed. In cases of closed wounds, the skin is intact and the underlying tissue is affected but not directly exposed to the outside environment. The following are the most common types of closed wounds:
Contusions – These are a common type of sports injury, where a direct blunt trauma can damage the small blood vessels and capillaries, muscles and underlying tissue, as well the internal organs or bone. Contusions present as a painful bruise with reddish to bluish discoloration that spreads over the injured area of skin.
Hematomas – These include any injury that damages the small blood vessels and capillaries resulting in blood collecting and pooling in a limited space. Hematomas typically present as a painful, spongy rubbery lump-like lesion. Depending on the severity and site of the trauama, hematomas can be small or large, deep inside the body or just under the skin.
Crush injuries – These are usually caused by an external high-pressure force that squeezes part of the body between two surfaces. The degree of injury can range from a minor bruise to a complete destruction of the crushed area of the body, depending on the site, size, duration and power of the trauma.
Causes of Acute Wound
Sudden forceful fall down
Road traffic accident
Burn and injured suddenly
Falls – Falling onto an outstretched hand is one of the most common causes of wound.
Sports injuries – Many sports injury occur during contact sports or sports in which you might fall onto an outstretched hand — such as in-line skating or snowboarding.
Motor vehicle crashes – Motor vehicle crashes can cause wound. Sometimes into many pieces, and often require surgical repair.
Have osteoporosis – a disease that weakens your bones.
Eave low muscle mass or poor muscle strength – or lack agility and have poor balance (these conditions make you more likely to fall)
Walk or do other activities in snow or on the ice – or do activities that require a lot of forwarding momenta, such as in-line skating and skiing
Wave an inadequate intake of calcium or vitamin D
Football or soccer, especially on artificial turf
Rugby
Horseback riding
Hockey
Skiing
Snowboarding
In-line skating
Jumping on a trampoline
Symptoms of Acute Wound
General signs and symptoms of a wound infection include
Increased firmness of skin or swelling around the wound bed
Increasing drainage from the wound bed
Delayed wound healing
Discoloration of the wound bed with it turning darker in color
Foul odor
Increased fragility of the wound bed
Wound breakdown /enlargement
The skin may harden or tighten in the area and red streaks may radiate from the wound. Wound infections may also cause fevers, especially when they spread to the blood.
Diagnosis of Acute Wound
Clinicians perform wound assessment as a means for determining the appropriate treatment for an extremely diverse grouping of disease processes. Just as hypertension is not treated the same as diabetes, each of the underlying etiologies of the given wound must be identified and treated as if it were its own disease, not a blanket classification of “wound.”[rx][rx]
The initial assessment should begin with the following:
How – How was the wound created and, if chronic, why is it still open? (underlying etiology)
Where – Where on the body is it located? Is it in an area which is difficult to offload, or to keep clean? Is it in an area of high skin tension? Is it near any vital structures such as a major artery?
When – How long has this wound been present? (eg., chronic or acute)
What – What anatomy does it extend? (e.g., epidermis, dermis, subcutaneous tissue, fascia, muscle, tendon, bone, arteries, nerves)
What – What co-morbidities or social factors does the patient have which might affect which might affect their ability to heal the wound?
Is it life threatening?
All of these factors significantly affect the treatment plan moving forward. While there are many excellent biologics, skin grafts, and other options available, without the appropriate understanding of the nature of the wound the chances of healing decline significantly.
Issues of Concern
While some wounds are simple, the majority of wounds many clinicians encounter are caused by or complicated by some other issue.[rx][rx][rx][rx] These are a few of the possible complications from different wound types:
A chronic wound will have a different makeup than that of an acute wound, requiring conversion for healing.
An underlying infection will prevent wound healing even if the infection is subacute.
A damaged or constricted arterial supply will prevent appropriate blood flow to the wound.
A damaged venous supply will cause venous stasis.
Physical pressure on chronic ulceration will cause repeated damage, preventing healing.
Tests
Many minor and superficial skin and wound infections are diagnosed by a healthcare practitioner based on a physical examination, sign and symptoms, and experience. A clinical evaluation cannot, however, definitively tell the healthcare practitioner which microbe is causing a wound infection or what treatment is likely to be effective. For that, laboratory testing is required.
Laboratory Tests
Examples of common tests include
Bacterial culture – This is the primary test used to diagnose a bacterial infection. Results are usually available within 24-48 hours.
Gram stain – This is usually performed in conjunction with the wound culture. It is a special staining procedure that allows bacteria to be evaluated under the microscope. The results are usually available the same day and provide preliminary information about the microbe that may be causing the infection.
Antimicrobial susceptibility – A follow-up test to a positive wound culture, this is used to determine the bacteria’s likely susceptibility to certain drugs and helps the healthcare practitioner select appropriate antibiotics for treatment. Results are typically available in about 24 hours. This testing can identify resistant bacteria such as MRSA.
Other tests may include
KOH prep – This is a rapid test performed to detect fungi in a sample. The sample is treated with a special solution, placed on a slide, and examined under a microscope.
Fungal culture – This is ordered when a fungal infection is suspected. Many fungi are slow-growing and may take several weeks to identify.
AFB testing – This is ordered when a mycobacterial infection is suspected. Most AFB are slow-growing and may take several weeks to identify.
Blood culture – This is ordered when infection from a wound may have spread to the blood.
Molecular testing – to detect genetic material of a specific microbe
Basic metabolic panel (BMP) or Comprehensive metabolic panel (CMP) – This may be ordered to detect underlying conditions that can affect wound healing, such as a glucose test to detect diabetes.
Complete blood count (CBC) – An elevated white blood cell (WBC) count may be a sign of infection.
Treatment of Acute Wound
Emergency Management
Pain control
Intravenous opiates are often used as patients typically in severe pain
Highly effective for management of pain
Lower side effect profile than systemic analgesia
Always calculate your toxic dose of local anesthetic to avoid local anesthetic systemic toxicity
Closed the wounds should be placed in long leg splint and can also be placed in traction
If open Fractures should receive antibiotics and should proceed to OR for irrigation/debridement.
Cleaning to remove dirt and debris from a fresh wound. This is done very gently and often in the shower.
Vaccinating for tetanus may be recommended in some cases of traumatic injury.
Exploring a deep wound surgically may be necessary. Local anaesthetic will be given before the examination.
Removing dead skin surgically. Local anaesthetic will be given.
Closing large wounds with stitches or staples.
Dressing the wound – The dressing chosen by your doctor depends on the type and severity of the wound. In most cases of chronic wounds, the doctor will recommend a moist dressing.
Relieving pain with medications – Pain can cause the blood vessels to constrict, which slows healing. If your wound is causing discomfort, tell your doctor. The doctor may suggest that you take over-the-counter drugs such as paracetamol or may prescribe stronger pain-killing medication.
Treating signs of infection including pain – pus and fever. The doctor will prescribe antibiotics and antimicrobial dressings if necessary. Take as directed.
Skin Traction (Hare or Thomas) if needed
May improve wound alignment, blood flow, and pain
Skin traction splint can cause complications if a patient with a significant injury (i.e. multi ligamentous knee injury)
Here we review only the commonly used medications that have a significant impact on healing, including glucocorticoid steroids, non-steroidal anti-inflammatory drugs, and chemotherapeutic drugs.
Glucocorticoid Steroids – Systemic glucocorticoids (GC), which are frequently used as anti-inflammatory agents, are well-known to inhibit wound repair via global anti-inflammatory effects and suppression of cellular wound responses, including fibroblast proliferation and collagen synthesis. Systemic steroids cause wounds to heal with incomplete granulation tissue and reduced wound contraction [rx]. Glucocorticoids also inhibit production of hypoxia-inducible factor-1 (HIF-1), a key transcriptional factor in healing wounds [rx].
Non-steroidal Anti-inflammatory Drugs – Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen are widely used for the treatment of inflammation and rheumatoid arthritis and for pain management. Low-dosage aspirin, due to its anti-platelet function, is commonly used as a preventive therapeutic for cardiovascular disease, but not as an anti-inflammatory drug [rx]. There are few data to suggest that short-term NSAIDs have a negative impact on healing.
Opioids – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.
Calcium & vitamin D3 – To improve bones health and healing fracture. As a general rule, men and women age 50 and older should consume 1,200 milligrams of calcium a day, and 600 international units of vitamin D a day.
Glucosamine & Diacerein, Chondroitin sulfate – can be used to tightening the loose tendon, cartilage, ligament, and cartilage, ligament regenerates cartilage or inhabits the further degeneration of cartilage, ligament.
Chemotherapeutic Drugs – Most chemotherapeutic drugs are designed to inhibit cellular metabolism, rapid cell division, and angiogenesis and thus inhibit many of the pathways that are critical to appropriate wound repair. These medications inhibit DNA, RNA, or protein synthesis, resulting in decreased fibroplasia and neovascularization of wounds [rx].
Nutrition – For more than 100 years, nutrition has been recognized as a very important factor that affects wound healing. Most obvious is that malnutrition or specific nutrient deficiencies can have a profound impact on wound healing after trauma and surgery. Patients with chronic or non-healing wounds and experiencing nutrition deficiency often require special nutrients. Energy, carbohydrate, protein, fat, vitamin, and mineral metabolism all can affect the healing process [rx].
Carbohydrates, Protein, and Amino Acids – Together with fats, carbohydrates are the primary source of energy in the wound-healing process. Glucose is the major source of fuel used to create the cellular ATP that provides energy for angiogenesis and deposition of the new tissues [rx]. The use of glucose as a source for ATP synthesis is essential in preventing the depletion of other amino acid and protein substrates [rx].
Protein – is one of the most important nutrient factors affecting wound healing. A deficiency of protein can impair capillary formation, fibroblast proliferation, proteoglycan synthesis, collagen synthesis, and wound remodeling. A deficiency of protein also affects the immune system, with resultant decreased leukocyte phagocytosis and increased susceptibility to infection [rx]. Collagen is the major protein component of connective tissue and is composed primarily of glycine, proline, and hydroxyproline. Collagen synthesis requires hydroxylation of lysine and proline, and co-factors such as ferrous iron and vitamin C. Impaired wound healing results from deficiencies in any of these co-factors [rx].
Arginine – is a semi-essential amino acid that is required during periods of maximal growth, severe stress, and injury. Arginine has many effects in the body, including modulation of immune function, wound healing, hormone secretion, vascular tone, and endothelial function. Arginine is also a precursor to proline, and, as such, sufficient arginine levels are needed to support collagen deposition, angiogenesis, and wound contraction [rx][rx]. Arginine improves immune function, and stimulates wound healing in healthy and ill individuals [rx]. Under psychological stress situations, the metabolic demand of arginine increases, and its supplementation has been shown to be an effective adjuvant therapy in wound healing [rx].
Glutamine – is the most abundant amino acid in plasma and is a major source of metabolic energy for rapidly proliferating cells such as fibroblasts, lymphocytes, epithelial cells, and macrophages [rx]. The serum concentration of glutamine is reduced after major surgery, trauma, and sepsis, and supplementation of this amino acid improves nitrogen balance and diminishes immunosuppression [rx]. Glutamine has a crucial role in stimulating the inflammatory immune response occurring early in wound healing [rx]. Oral glutamine supplementation has been shown to improve wound breaking strength and to increase levels of mature collagen [rx].
Fatty Acids – Lipids are used as nutritional support for surgical or critically ill patients to help meet energy demands and provide essential building blocks for wound healing and tissue repair. Polyunsaturated fatty acids (PUFAs), which cannot be synthesized de novo by mammals, consist mainly of two families, n-6 (omega-6, found in soybean oil) and n-3 (omega-3, found in fish oil). Fish oil has been widely touted for the health benefits of omega-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The effects of omega-3 fatty acids on wound healing are not conclusive. They have been reported to affect pro-inflammatory cytokine production, cell metabolism, gene expression, and angiogenesis in wound sites [rx] . The true benefit of omega-3 fatty acids may be in their ability to improve the systemic immune function of the host, thus reducing infectious complications and improving survival [rx].
Vitamins, Micronutrients, and Trace Elements – Vitamins C (L-ascorbic acid), A (retinol), and E (tocopherol) show potent anti-oxidant and anti-inflammatory effects. Vitamin C has many roles in wound healing, and a deficiency in this vitamin has multiple effects on tissue repair. Vitamin C deficiencies result in impaired healing, and have been linked to decreased collagen synthesis and fibroblast proliferation, decreased angiogenesis, and increased capillary fragility. Also, vitamin C deficiency leads to an impaired immune response and increased susceptibility to wound infection [rx;rx]. Similarly, vitamin A deficiency leads to impaired wound healing. The biological properties of vitamin A include anti-oxidant activity, increased fibroblast proliferation, modulation of cellular differentiation and proliferation, increased collagen and hyaluronate synthesis, and decreased MMP-mediated extracellular matrix degradation [rx].
Vitamin E, an anti-oxidant – maintains and stabilizes cellular membrane integrity by providing protection against destruction by oxidation. Vitamin E also has anti-inflammatory properties and has been suggested to have a role in decreasing excess scar formation in chronic wounds. Animal experiments have indicated that vitamin E supplementation is beneficial to wound healing [rx, rx; rx] and topical vitamin E has been widely promoted as an anti-scarring agent. However, clinical studies have not yet proved a role for topical vitamin E treatment in improving healing outcomes [rx,rx].
Several micronutrients – have been shown to be important for optimal repair. Magnesium functions as a co-factor for many enzymes involved in protein and collagen synthesis, while copper is a required co-factor for cytochrome oxidase, for cytosolic anti-oxidant superoxide dismutase, and for the optimal cross-linking of collagen. Zinc is a co-factor for both RNA and DNA polymerase, and a zinc deficiency causes a significant impairment in wound healing. Iron is required for the hydroxylation of proline and lysine, and, as a result, severe iron deficiency can result in impaired collagen production [rx,rx;rx, rx; rx].
Normal Wound-healing Process
Phase
Cellular and Bio-physiologic Events
Hemostasis
vascular constriction
platelet aggregation, degranulation, and fibrin formation (thrombus)
Inflammation
neutrophil infiltration
monocyte infiltration and differentiation to macrophage
lymphocyte infiltration
Proliferation
re-epithelialization
angiogenesis
collagen synthesis
ECM formation
Remodeling
collagen remodeling
vascular maturation and regression
Dressing
Some of the unique features of each are described below.
The following dressings may be used on chronic or acute wounds depending on the nature of the wound.
Low or nonadherent dressings – are inexpensive and allow wound exudate to pass through into a secondary dressing while helping to maintain a moist wound environment. These dressings are specially designed to reduce adherence to the wound bed. Non adherent dressings are made from open weave cloth soaked in paraffin, textiles, or multilayered or perforated plastic films. This type of dressing is suitable for flat, shallow wounds with low exudate such as a venous leg ulcer.
Hydrocolloid dressings – are composed of adhesive, absorbent, and elastomeric components. Carboxymethylcellulose is the most common absorptive ingredient. They are permeable to moisture vapor, but not to water. Additionally, they facilitate autolytic débridement, are self-adhesive, mold well, provide light-to-moderate exudate absorption, and can be left in place for several days, minimizing skin trauma and disruption of the healing process. They are intended for use on light-to-moderate exuding, acute or chronic partial- or full-thickness wounds but are not intended for use on infected wounds. Upon sustained contact with wound fluid, the hydrocolloid forms a gel.
Foam dressings – vary widely in composition and construction. They consist of a polymer, often polyurethane, with small, open cells that are able to hold fluids. Some varieties of foam dressings have a waterproof film covering the top surface and may or may not have an adhesive coating on the wound contact side or border. Foams are permeable to water and gas, and are able to absorb light to heavy exudate. This type of dressing is frequently used under compression stockings in patients with venous leg ulcers.
Film dressings consist of a single – thin transparent sheet of polyurethane coated on one side with an adhesive. The sheet is permeable to gases and water vapor but impermeable to wound fluids. Film dressings retain moisture, are impermeable to bacteria and other contaminants, allow wound observation, and do not require a secondary dressing. Excessive fluid buildup may break the adhesive seal and allow leakage. Film dressings are intended for superficial wounds with little exudate and are commonly used as a secondary dressing to attach a primary absorbent dressing. The dressing may remain in place for up to seven days if excessive fluid does not accumulate. Film dressings have been used extensively to treat split-thickness graft donor sites.
Alginate dressings – are made from calcium or calcium-sodium salts of natural polysaccharides derived from brown seaweed. When the alginate material comes into contact with sodium-rich wound exudates, an ion exchange takes place and produces a hydrophilic gel. This hydrophilic gel is capable of absorbing up to 20 times its weight and does not adhere to the wound. This dressing can remain in place for about seven days if enough exudate is present to prevent drying. This category of dressing is best suited for moist, moderate-to-heavy exuding wounds. Alginate dressings require a secondary dressing, such as a film dressing, to hold them in place and to prevent the alginate from drying out.
Hydrofiber dressing – is composed of sodium carboxymethylcellulose fibers.[rx] The fibers maintain a moist wound environment by absorbing large amounts of exudate and forming a gel. This dressing is not intended for lightly exuding wounds. A secondary dressing is required.
Hydrogel sheets – are three-dimensional networks of cross-linked hydrophilic polymers. Their high water content provides moisture to the wound, but these dressings can absorb small-to-large amounts of fluid, depending on their composition. Depending on wound exudate levels, hydrogels may require more frequent dressing changes, every 1–3 days, compared with other synthetic dressings. Hydrogel sheets can be used on most wound types but may not be effective on heavily exuding wounds. The gel may also contain additional ingredients such as collagens, alginate, or complex carbohydrates. Amorphous hydrogels can donate moisture to a dry wound with eschar and facilitate autolytic débridement in necrotic wounds. A second dressing may be used to retain the gel in shallow wounds.
Polymer-based dressing – Transforming methacrylate (TMD) was compared to carboxymethylcellulose (CMC-Ag) in one study of 34 patients. The study showed that TMD, compared to CMC-Ag, was associated with lower pain scores and better patient satisfaction, but the two dressings did not differ in terms of number of dressing changes and the time to complete healing.[rx] Suprathel (a polymer-based dressing) was evaluated in a study of 72 patients, and it was compared to a polyurethane dressings (Biatain-Ibu) and a silicone dressing (Mepitel). The three dressings had similar time to re-epithelialization, but Suprathel had a significantly lower number of dressing changes compared to the two other dressings.[rx]
Crystalline cellulose dressings – Results for the comparison between CMC-Ag and TMD are presented above.[rx] Veloderm was compared to Vaseline gauze in 96 patients.[rx] The study showed that Veloderm was associated with lower time to complete healing and number of dressing changes. The two dressings did not differ in terms of incidence of exudate, peri-lesional erythema or pain intensity.[rx]Rayon dressing was compared to Veloderm in a study of 14 patients and 28 skin graft donor sites.[rx] Rayon dressing showed lower dressing adherence to wound and lower 1st day pain score; the two dressings did not differ in terms of pain beyond day 14, hyperemia, edema and pruritus.[rx]
Alginate dressings – The study evaluated the dressing materials in terms of time to healing, pain scores, clinical infections and hypergranulation. Results showed that the six types of dressings did not differ with statistical significance except in the following cases: first, the semi-permeable films (Tegaderm or Opsite) were associated with lower pain scores than any other dressing type; second, the hydrocolloid dressing (DuoDerm E) required lower time (seven days difference) to healing than all other dressings; finally, the gauze dressings (Adaptic or Jelonet) were associated with the highest incidence of clinical infections.[rx]
Alginate-based dressings – were also evaluated in three other trials; the first one compared Algisite to a keratin dressing (Keramatrix).[rx]The trial showed that Algisite was associated with higher rate of epithelialization seven days after the operation than Keramatrix in patients older than 50 years; for younger patients, the rate of epithelialization did not significantly differ.[rx] Ding et al. compared time to healing and pain scores between alginate-silver dressing and hydrofiber dressing (Aquacel-A) in 10 patients and 20 donor sites; the results showed that the alginate dressing was associated with shorter time to healing and lower pain scores.[rx]The third trial compared Algisite covered by a polyurethane dressing (Opsite) to paraffin gauze dressing; the results showed that the two dressings did not differ in terms of pain scores, time to epithelialization and the assessment of general comfort. Algisite dressings required more dressing changes (34 times) than the paraffin gauze (4 times).[rx]
Polyurethane dressings – Opsite and Tegaderm films were evaluated in Brolemann’s study, and the results were presented above. Another trial compared the Opsite dressing to a hydrofiber dressing (Aquacel-A); the results showed that Opsite was associated with lower scores of pain.[rx] The Biatain-Ibu dressing was compared to Suprathel (polymer dressing) and Mepitel (silicone dressing); the results were presented above with polymer-based dressings.[rx] Another study compared Biatain-Ibu to a gauze dressing (Jelonet), and it was reported that Biatain-Ibu was associated with lower pain and itching than Jelonet; however, the study did not report any statistical testing for the differences between interventions.[rx]
Gauze dressings – Gauze dressings were evaluated in seven trials; the results of four trials were reported earlier in this section,[rx,rx,rx,rx]and the remaining three trials were as follows one trial compared Xeroform (gauze dressing) to a multilayer dressing and showed that Xeroform was associated with longer healing time and higher pain scores than Oxyband.[rx]The second trial compared paraffin gauze to a hydrofiber dressing (Aquacel) and reported that the paraffin gauze was associated with longer re-epithelialization time and higher pain score during dressing.[rx]The last trial compared Jelonet to a multilayer dressing as a dressing over a skin graft (receiver site); the results showed that the two dressings did not affect the time to graft take, number of nursing interventions, or post-operative infections; however, they showed that Jelonet was associated with higher pain score at the time of dressing removal.[rx]
Hydrocolloid dressings – The efficacy of DuoDerm E was compared to six other dressing materials in Brolmann’s trial; the results of this trial were presented earlier in this section.[rx]In another trial, DuoDerm was compared to a silicone-based dressing (AWBAT-D); the trial showed that the two dressings did not differ in terms of pain scores, wound size or time to discharge, but the DuoDerm was associated with shorter time to re-epithelialization.[rx]
Hydrofiber dressings – The efficacy of Aquacel was studied in six trials; the results of four trials were presented earlier in the section.[rx,rx,rx,rx]One of the remaining trials compared Aquacel to carbohydrate wound dressing (Glucan II), and it showed that the two interventions did not differ in terms of time to re-epithelialization, pain scores, or donor site infection.[rx]The second trial compared two different protocols of using Aquacel; in the first protocol, Aquacel dressing was covered with gauze, while in the second one, it was covered with polyurethane film (OpSite).[rx] The trial reported that the second protocol was associated with a larger number of donor sites healing at day 14 after surgery (88% versus 67%), and it was associated with lower pain during mobility the first day after operation; the two dressings did not differ in pain scores during rest at all time-point evaluations.[rx]
Silicone dressings – Four trials evaluated the efficacy of silicone-based dressings; the result three of trials were presented earlier in this section.[rx,rx,rx] The fourth trial compared Mepitel dressing to a nylon dressing (Bridal veil) when used over a skin graft (receiver site).[rx] The results of this trial showed that Mepitel dressing was associated with less pain, easier use, and better overall experience for patients.[rx]
Keratin dressings – The efficacy of Keranatrix was evaluated in one study the results of which were presented earlier in this section.[rx]
Self-adhesive fabric dressing (Mefix) with or without fibrin sealant – One trial evaluated the difference between using Mefix alone or with a fibrin sealant; the trial showed that the use of fibrin sealant was associated with lower daily pain and incapacity scores, but it did not affect the time to dressing removal or the time to discharge for the hospital.[rx]
Multilayer (combination) dressings – The efficacy of Oxyband and Allyven was evaluated in two studies the results of which were presented earlier in this section.[rx,rx]
Nylon dressings – The efficacy of Bridal veil was evaluated in one study the results of which were presented earlier in this section.[rx]
Carbohydrate wound dressings – The efficacy of Glucan dressing was evaluated in one study the results of which were presented earlier in this section.[rx]
Negative pressure dressings – One trial compared negative pressure dressings with a conventional dressing with gauze; both dressings were used over skin grafts (receiver sites).[rx]The trial reported that the negative pressure dressing was associated with a higher percentage of graft take and shorter duration of dressing.[rx]
Complication of Wound Healing
Factors that can slow the wound healing process include
Dead skin (necrosis) – dead skin and foreign materials interfere with the healing process.
Infection – an open wound may develop a bacterial infection. The body fights the infection rather than healing the wound.
Haemorrhage – persistent bleeding will keep the wound margins apart.
Mechanical damage – for example, a person who is immobile is at risk of bedsores because of constant pressure and friction.
Diet – poor food choices may deprive the body of the nutrients it needs to heal the wound, such as vitamin C, zinc and protein.
Medical conditions – such as diabetes, anaemia and some vascular diseases that restrict blood flow to the area, or any disorder that hinders the immune system.
Age – wounds tend to take longer to heal in elderly people.
Medicines – certain drugs or treatments used in the management of some medical conditions may interfere with the body’s healing process.
Smoking – cigarette smoking impairs healing and increases the risk of complications.
Varicose veins – restricted blood flow and swelling can lead to skin break down and persistent ulceration.
Dryness – wounds (such as leg ulcers) that are exposed to the air are less likely to heal. The various cells involved in healing, such as skin cells and immune cells, need a moist environment.
What is the best vacuum cleaner to buy?
5 Best Vacuum Cleaner
Pool Vacuum Heads – Types and How To Buy It
