Carbs, Fats, and Proteins: How the Body Burns Fuel


In its simplest terms, metabolic biochemistry is “fuel in, energy out”. The energy gained from burning fuel (ie: food) is used to drive all the processes going on in your body. These include the building of proteins, DNA (your genetic material), and fat, as well as mechanical things like muscle contraction.

Fuel for the human body takes three basic forms: carbohydrates (sugars), protein, and fat. Humans are capable of burning all three of these fuels, but do so at different times, rates, and under different circumstances. Using an extreme example, under starvation conditions the body burns its fat stores. Once fat stores are depleted the body begins digesting non-essential proteins and then essential proteins, which ultimately leads to organ damage and death. Thankfully, the body is relatively efficient and uses the best available fuel first before it has to tap into essential reserves.


Let’s start by discussing carbohydrates. Carbohydrates, or “carbs”, are simply sugar molecules linked to one another in varying arrangements. For example, starch, the most important carbohydrate in the human diet, is nothing more than numerous glucose molecules linked together in a long strand. Potatoes are an excellent example.

Another example of a carbohydrate is glycogen. Glycogen is how humans store excess glucose (a single sugar molecule) for later use. Unlike starch, which is a long chain of individual glucose molecules, glycogen is a highly branched structure that allows the body to rapidly cleave off individual sugar molecules to be burned for energy.

Carbohydrates can be further broken down into 2 categories: simple and complex. We’ve all heard of the term “complex carbohydrates”, which is a fancy way of saying multiple sugar molecules linked together in a complicated way. Contrarily, a simple carbohydrate is merely a few (usually 1 to 3) sugar molecules linked together.

Why make the distinction between simple and complex carbs? For starters, simple carbohydrates are rapidly absorbed by the gut and enter the bloodstream very quickly. Candy bars are a great example! If you need a quick boost of energy unwrap a Snickers®!

The problem is that since simple carbs enter the bloodstream so rapidly they get metabolized quickly. This causes you to lose that energy boost fast, which is why you often feel “de-energized” an hour or so after eating "junk food". In contrast, complex carbs get degraded by the gut much less rapidly, and therefore slowly trickle into the bloodstream. This gives you a more sustained, but less pronounced energy boost. Whole grains are a great example of complex carbs.

Why all the hub-bub about carbohydrates? Because they are, for the most part, the first energy source that is utilized during exercise. This forms the basis behind “carbo loading”, or eating a meal rich in carbohydrates the night before, or morning of, a planned work out. During exercise, the body will then utilize the individual sugar molecules in the carbohydrates to provide energy for your muscles and brain. Once you run out of sugar (or the form that humans store it in, glycogen) your body turns to the other fuel sources, namely, protein and fat.


The next fuel that gets burned is fat. All human beings have a certain percentage of body weight that is fat. From an evolutionary stand point this is advantageous. During times of drought or famine there was not enough food to provide reliable carbohydrate or protein, and thus humans survived by “burning” their fat stores. In biochemical terms, fat is nothing more than long chains of carbon atoms linked together. Suffice it to say that it is the carbon in the fat that gets utilized to form energy that your muscles and other body tissues use.

Why not burn fat first? Because fat is not as efficient an energy provider as sugar. This is the reason that endurance athletes, a few hours into a work out, hit the proverbial “wall”. The wall represents the point where they have burned up all the carbohydrate in their body, and are now running on fat reserves. The decreased amount of energy gained per unit of fat, when compared to what you get with carbs, results in a relative feeling of fatigue.

These principles can also be used as a weight loss system. Using the basics of carbohydrate and fat metabolism it makes sense that people have difficulty losing weight when they exercise vigorously for only half an hour. This is because the quick vigorous exercise burns mostly carbohydrate stores in the liver (ie: glycogen); the body never touches its fat reserves!

In contrast, running a marathon (or a nice long walk or jog in the park) causes the body to tap into its fat reserves. This is also the idea behind exercising early in the morning before having breakfast. In the morning your body has been burning carbohydrates to keep all your organs functioning; therefore, in the morning your body has less carbohydrate available to burn because it was slowly getting eaten away during sleep. If you exercise at this point you’ll have to tap into your fat stores earlier than you normally would.


The third and final fuel is protein. The body rarely burns protein as its sole fuel source, and when it does it is usually under conditions of starvation. Interestingly, when no carbohydrate is present in the diet, the body will use the amino acid backbones of protein to form glucose (a carbohydrate) in order to supply the brain with adequate energy.

It was once thought that protein provided the energy that athletes used during exercise. This was the basis behind the “steak-and-eggs” breakfast prior to an athletic event. This has fallen out of favor as biochemists (and athletes) now realize that the body prefers to burn carbohydrates, then fat, and finally protein if all else fails.


The three main fuel sources in humans are carbohydrates, fats, and proteins. They are used preferentially under different conditions. In general, the body burns carbohydrates, then fats, and then proteins, in that order.

It is important to realize that energy metabolism is not an "all-or-none" phenomenon. The body is constantly fine tuning the exact blend of carbohydrate, fat, and protein metabolism to ensure the appropriate supply of energy to the bodies tissues.

References and Resources

  • Champe PC. Lippincott’s Illustrated Reviews: Biochemistry. Second Edition. Lippincott-Ravens Publishers, 1992.
  • Nelson DL, Cox MM. Lehninger Principles of Biochemistry. Fifth Edition. New York: Worth Publishers, 2008.
  • Summerbell CD, Cameron C, Glasziou PP. WITHDRAWN: Advice on low-fat diets for obesity. Cochrane Database Syst Rev. 2008 Jul 16;(3):CD003640.
  • Elliott SA, Truby H, Lee A. Associations of body mass index and waist circumference with: energy intake and percentage energy from macronutrients, in a cohort of Australian Children. Nutr J. 2011 May 26;10(1):58. [Epub ahead of print]

Starling the Darling: Starling’s Equation and Fluid Movement

Starling’s equation quantifies the movement of fluid into and out of a capillary as a result of filtration. It is based on two important variables: hydrostatic and oncotic pressure.

But before getting too scientific, let’s get back to the basics… Capillaries are the tinniest blood vessels in the body. They are the main site of gas and nutrient exchange for the tissues that they serve.

The fluid (ie: blood) inside the capillaries has a particular pressure associated with it. This is known as the “hydrostatic” pressure. In addition, there are numerous proteins floating around in the blood. These proteins determine the “oncotic” pressure.

Fluid, and to some degree proteins, are able to seep into and out of the capillary. However, the amount of “seepage” is based not only on the capillaries’ hydrostatic and oncotic pressure, but also on the hydrostatic and oncotic pressure of the surrounding tissues.

The tissue surrounding capillaries is composed of cells and their supporting structures. Depending on the particular tissue type, the supporting structures are generally proteins like collagen and long chain carbohydrate molecules known as proteoglycans. All of these molecules are collectively referred to as the “cellular interstitium”. The interstitium is where fluid seeps into and out of the capillary network.

The Equation

Taking the hydrostatic and oncotic pressures of the blood and interstitium into account we can predict which way fluid will move: in to or out of the capillary. This can be done numerically as shown in the following equation:

Driving pressure across capillary wall ≡
(PHS capillary – PHS interstitum) – (PO capillary – PO interstitium)

HS = hydrostatic pressure
O = oncotic pressure

If this number is positive, it means that fluid wants to leave the capillary and enter the interstitium (ie: there is a large driving pressure trying to push fluid out of the capillary); if it is negative, it means that fluid wants to leave the interstitium and re-enter the capillary.

Now to throw a monkey wrench into the equation… Although the hydrostatic and oncotic pressures are the main driving forces there are two additional factors that must be taken into account.

The first of these factors is the filtration co-efficient. It is based on how large and “leaky” the capillary wall is. Simply stated, if the capillary wall is large and leaky then more fluid can be filtered across it, duh! Increased leakiness can be caused by many different things such as histamine release (ie: allergies), mechanical damage to the capillary, etc.

The second factor that can alter the above equation is known as the reflection co-efficient. It is based on the fact that some proteins from the blood are able to cross the vessel wall into the interstitium. This effectively reduces the oncotic pressure within the capillary, and increases the oncotic pressure within the interstitium. Suffice it to say that different capillary beds have different reflection co-efficients depending on which organ system is being studied.

Taking everything into account we get the following equation:

Driving pressure across capillary wall ≡
Kf(PHS capillary – PHS interstitum) – σ(PO capillary – PO interstitium)

HS = hydrostatic pressure
O = oncotic pressure
Kf = filtration co-efficient
σ = reflection co-efficient


Starling’s equation predicts how much fluid will be filtered into, or out of, a capillary. It is based on four things: oncotic pressure, hydrostatic pressure, the reflection co-efficient, and the filtration co-efficient.

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References and Resources

Pitting Edema or Look How Swollen My Legs Are

Pitting edema is a physical examination finding that occurs when you press on a patient’s skin, usually the shins, ankles, or feet, and a “pit” forms at the site of pressure.

Pitting edema is graded on a scale from 1 to 4, which is based on both the depth the “pit” leaves and how long the pit remains. A patient with a score of 1 has edema that is slight (roughly 2mm in depth) and disappears rapidly. A score of 2 is deeper (4mm) and disappears within 15 seconds. A score of 3 is deeper yet (6mm), and can last longer than a minute; in stage 3 pitting edema the extremity also looks grossly swollen. Finally, stage 4 is the most severe with deep pitting (8mm or greater in depth) that may last more than 2 minutes.


Pitting edema is most commonly seen in patients with heart, liver, or kidney failure. These three conditions cause the body to hold onto excess sodium and water. It can also be seen in patients with rheumatological diseases such as rheumatoid arthritis and systemic lupus erythematosus. Pitting edema can also be seen in patients receiving excess intravenous fluids.

Regardless of the cause, the excess fluid leaks out of the capillaries and into the surrounding tissues. When it leaks into the subcutaneous tissues it is seen clinically as pitting edema. Patients with pitting edema can also suffer from pulmonary edema as well as ascites.


Pitting edema occurs when the examiner can make an indentation or “pit” in the extremity of a patient. This is caused by excessive fluid seeping out of the capillaries and into the subcutaneous tissues. It occurs most commonly in patients with heart, kidney, or liver failure, as well as in patients who have received too much intravenous fluid.

Related Articles

References and Resources

How To Systematically Interpret a Head CT: Blood Can Be Bad

Head CTs are a common, inexpensive, and fast way of evaluating intracranial pathology. Although they do not give the anatomical detail of an MRI, they are still extremely important in diagnosing “gross” pathology that needs emergent intervention.

CT scans are based on the Hounsfield unit (HU), which is an indirect way to measure density. Interestingly, Sir Godfrey Newbold Hounsfield won a Nobel prize for his work on developing the CT scanner, but I digress…

The importance of the Hounsfield unit is that things that are hyper-dense (very dense) appear bright; those things that are hypo-dense (not very dense) appear dark. The different tissues and fluids within the confines of the skull have varying densities. The most dense materials, like bone, have very high Hounsfield units; less dense materials such as air and cerebrospinal fluid have very low Hounsfield units.

It is important to approach head CTs in a systematic fashion so that subtle (and not so subtle) pathology is not missed. The easiest way I have found to read a head CT is to remember the following mnemonic:

Blood Can Be Very Bad

The first “B” in the mnemonic stands for, you guessed it, blood. There are five different pathological locations that blood can be located: epidural, subdural, subarachnoid, intraventricular, and intraparenchymal. Depending on the age of the blood, it may be hyper-dense (acute/active bleeding), isodense (roughly 3 to 7 days old), or hypo-dense (older than 7 days).

CT scans of Intracerebral Hemorrhages
The "C" in the mnemonic stands for "cisterns". Cisterns are enlarged subarachnoid spaces where cerebrospinal fluid pools. The most important cisterns are around the brainstem. They include the interpeduncular, suprasellar, ambient, quadrigeminal and pre-pontine cisterns. A healthy amount of cerebrospinal fluid should “bathe” the brainstem; if there is increased intracranial pressure cerebrospinal fluid will get pushed out of these cisterns as brain tissue starts to herniate into them. And that as they say is “no bueno”.

The second "B" stands for "brain". Although blatant pathology such as blood clots are usually readily apparent, more subtle pathology can also be obtained from a CT. For example, blurring of the gray-white junction may indicate evolving stroke. Any areas of hypodensity (ie: dark areas) within the brain may indicate edema associated with a tumor.

The "V" represents the ventricular system. The ventricular system consists of a pair of lateral ventricles, a third ventricle, and a fourth ventricle (don’t ask me what happened to the first and second ventricle!). The ventricles are in communication with one another via holes known as foramen. The paired foramen of Monroe connect the lateral ventricles to the third ventricle; the cerebral aqueduct of Sylvius connects the third ventricle to the fourth ventricle. The fourth ventricle drains into the subarachnoid space surrounding the spinal cord via the foramen of Magendie and Lushka.

The ventricular system is quite symmetric. Any obvious asymmetries may indicate a pathologic process "pushing" on a ventricle causing it to become distorted. In addition, if the ventricles are larger than normal it may indicate the presence of hydrocephalus, a condition in which cerebrospinal fluid is not reabsorbed appropriately.

The final "B" in the mnemonic stands for "bone". The skull should be assessed for fractures, especially in trauma patients. A common place for fractures is at the skull base. Time should be spent assessing this area to rule out fractures that extend across the canals and foramen that house the carotid arteries, jugular veins, and cranial nerves.

Reading a head CT is the first step in determining what additional imaging studies are necessary, or what treatment should be given. By using the above mnemonic it allows the interpreter of the scan to quickly and effectively assess if there is underlying pathology that needs further evaluation.


The mnemonic – blood can be very bad – can be used to systematically interpret a head CT. The first "B" stands for blood. The "C" stands for cisterns. The second "B" stands for brain. The "V" represents the ventricular system. And the last "B" stands for bone. By looking at these five components it is possible to assess all the important pathology that may require further imaging and/or treatment.

References and Resources

Chiari Malformation: Type1, Tonsils and Syrinx

The Chiari malformations are a group of disorders characterized, at least in part, by herniation of hindbrain structures through the foramen magnum at the base of the skull. They are categorized as type 1, type 2, and type 3 depending on clinical and radiographic findings.

This article will focus on type 1 Chiari malformations. The definition of this malformation has been debated, but most agree that the combination of herniated cerebellar tonsils (usually defined as greater than 5mm below the foramen magnum), with or without a syrinx, in the setting of referable symptoms is sufficient to make the diagnosis.

So why do the cerebellar tonsils herniate? Nobody knows for sure! We do know that type 1 malformations can be congenital or acquired. One theory is that tonsillar herniation is a result of an abnormally small posterior fossa (ie: the bones that compose the base of the skull). A small posterior fossa may be caused by under-development of the occipital somites in-utero (the fetal precursors that form bone and connective tissues), premature fusion of the cranial bones (ie: craniosynostosis), or medical conditions that promote abnormal bony growth.

Other experts advocate that abnormal cerebrospinal fluid pressures between the brain and spine may cause the tonsils to herniate downwards.

Regardless of how you slice it, we can say with certainty that there are multiple potential etiologies for type 1 Chiari malformations.

Type 1 Chiari malformations are commonly associated with a finding known as a “syrinx”. A syrinx is an abnormal fluid filled cavity that is seen in the cervical and/or thoracic spinal cord. It may represent an enlargement and extension of the central canal of the cord, in which case it is termed hydromyelia; it may also represent a complex glial lined cavity, which is referred to as syringomyelia. Regardless, syrinxes are found in 30% to 70% of type 1 Chiari malformations.

For unclear reasons, type 1 Chiari malformations with a syrinx are associated with scoliotic curves of the spine (especially left sided curves). It is believed that the syrinx puts pressure on the motor pathways of the spinal cord. This results in weakness of the paraspinal muscles causing the vertebral column to curve.

Signs and Symptoms

The most common presenting symptom of a type 1 Chiari malformation is pain. The pain is usually located at the back of the head and upper neck. Additionally, a cape-like sensation loss, as well as problems with vision and/or hearing may also be present.

Myelopathic signs or symptoms may be present if there is a syrinx. Myelopathic patients present with a combination of gait dysfunction, hand clumsiness, weakness, abnormally brisk reflexes, spasticity, and Lhermitte’s sign.


Type 1 Chiari Malformation
Diagnosis of a type 1 Chiari malformation is made when an MRI shows abnormal herniation of the cerebellar tonsils, with or without an associated syrinx, in the context of appropriate signs and/or symptoms.


The treatment of Chiari malformation is with surgical decompression. Most commonly this involves "shaving" off part of the occipital bone and removing the C1 lamina. This effectively decompresses the spinal cord and cerebellar tonsils.

If an associated syrinx is present, many neurosurgeons will open the dura (ie: the lining of the spinal cord) and perform a "duraplasty"; during the duraplasty a patch is sewn into place to give the spinal cord and cerebellar tonsils more room. Duraplasty generally improves the size and severity of the syrinx over time, but adds risk and complications to the procedure.

Some neurosurgeons will surgically shrink the cerebellar tonsils after opening the dura. This is done with bipolar electrocautery and serves to further decompress the area.


Type 1 Chiari malformations are hindbrain abnormalities characterized by herniation of the cerebellar tonsils below the foramen magnum. They are associated with cervicothoracic syrinxes as well as neuromuscular scoliosis. Symptoms can range from pain to neurological deficits. Treatment is with surgical decompression, although the exact type of decompression has been the subject of intense research.

References and Resources

Pneumothorax: Visceral and Parietal Pleura and a Little Air In Between

In order to understand what a pneumothorax is we have to first appreciate the anatomy of the lung and its surrounding tissues.

The lung is enveloped by two layers of connective tissue known as the visceral and parietal pleura. The visceral pleura is directly connected, and immediately adjacent to the lungs. The parietal pleura sits on top of the visceral pleura like a blanket, but is not, in the strictest sense of the word, attached to the visceral pleura.

This unique arrangement creates a potential space between the visceral and parietal layers. Normally this space is empty and the layers of pleura sit directly on top of one another. However, in some instances air can dissect into that potential space. When this occurs it is called a “pneumothorax”.


A pneumothorax is classified as either “simple” or “tension”. A tension pneumothorax occurs when a progressively larger amount of air gets trapped in the space between the parietal and visceral pleural layers.

Tension pneumothoraces occur when the pathology causing the pneumothorax creates a one way valve mechanism allowing air into, but not out of the pleural space. With each breath more air is drawn into the pneumothorax, but is unable to escape. The end result is progressive enlargement of the pneumothorax. As a result, the air pushes the heart and mediastinal structures to the opposite side of the chest. And this is no bueno.

On the other hand, a simple pneumothorax is present when the amount of air remains stable, and there is no shift of mediastinal structures.


Anything that introduces air between the parietal and visceral pleura can cause a pneumothorax. Trauma is a common cause of pneumothorax and can occur if the chest wall is damaged or a bronchus ruptures. Subpleural blebs, which are basically small “air blisters” on the surface of the lung are also common causes of non-traumatic pneumothorax. Patients who smoke, or who have underlying connective tissue diseases such as Marfan’s syndrome are at increased risk of developing a pneumothorax. For unclear reasons, spontaneous pneumothorax is often seen in tall, thin, white males.

Signs and Symptoms

Signs and symptoms are usually dependent on the size of the pneumothorax. One common symptom is “pleuritic” chest pain. This is caused by air irritating the parietal pleura; this type of pain is usually worse when the patient takes a breath. Patients also commonly complain of dyspnea (ie: shortness of breath).

On physical exam the patient will have decreased or absent breath sounds over the area of the pneumothorax. In addition, if you percuss (ie: tap) the patient’s lung with your finger it will sound hyper-resonant. In tension pneumothoraces the air may push on heart structures leading to tachycardia (ie: increased heart rate) and hypotension (ie: decreased blood pressure).


The quickest way to diagnose a pneumothorax is with a chest x-ray. There are several things you should look for when attempting to diagnose a pneumothorax based on an x-ray.

The first is absence of lung markings. However, this is not a fool proof system because lung markings may be absent in other diseases of the lung such as bullae. You also need to see a white line that parallels the chest wall. This is known as the "pleural white line", which represents separation of the visceral and parietal pleura. Additionally, in a tension pneumothorax the heart structures and trachea will deviate away from the pneumothorax.


Treatment is dependent on the size of the pneumothorax and whether or not the patient has symptoms. Small (ie: less than 3cm between the chest wall and lung tissue) and asymptomatic lesions can be treated conservatively with supplemental oxygen via a nasal cannulae or face mask.

If the pneumothorax is larger than 3cm, or the patient has symptoms, a needle can be used to aspirate the air out of the chest. If this fails to re-inflate the lung, the patient will likely have to have a chest tube placed. In addition, any patient who is clinically unstable should have a chest tube placed.

Tension pneumothoraces are treated emergently by inserting a large bore needle into the 2nd intercostal space at the midclavicular line. This allows trapped air to escape through the newly created needle hole and prevents further air trapping.


A pneumothorax occurs when air dissects between the visceral and parietal pleural layers that envelope the lung. There are numerous causes. Symptoms include chest pain and shortness of breath although small pneumothoraces may be asymptomatic. Diagnosis is generally made from a chest x-ray. Treatment depends on symptomatology and the size of the pneumothorax.

References and Resources

Gout: Uric Acid, Negatively Birefringent, and My Big Toe

Gout occurs when uric acid crystals form in joint spaces. Everyone has some level of uric acid in their blood stream. However, it is only when the level becomes high enough that uric acid leeches into the joint spaces and crystallizes. Once there, the crystals cause signifcant inflammationand the affected joint becomes painful, red, and swollen.

The causitive agent, uric acid, is a by product of purine catabolism. Purines are an important component of nucleotides, which are the building blocks of DNA and RNA. Purines are also seen in molecules like adenosine triphosphate, which serves as a source of cellular energy. The final product of the degradation of these molecules is, you guessed it, uric acid!

The degradation pathway for both adenine and guanine (and their constituent molecules) are shown below. The key enzymes involved in this degradation are shown in red.

Purine Catabolism

When uric acid is formed, the kidneys filter it, and then excrete it into the urine. Some people are predisposed to either under-secrete or over-produce uric acid. In either case it builds up in the blood stream. This is known as "hyperuricemia". In some people hyperuricemia can cause gout. However, it is important to note that not everyone with hyperuricemia develops gout.


Gout Crystals

An official diagnosis of gout can only be made by tapping the joint (ie: sticking a needle into the joint and aspirating the contents) and looking at the fluid under a microscope.

If uric acid crystals are present, they will be "negatively birefringent", which means that they appear yellow under a parallel light source. Interestingly, if the light source is turned perpendicular the crystals turn blue (this is the exact opposite of pseudogout, which is discussed in another article).

Often times clinicians will order a blood uric acid test. In an acute attack, uric acid levels are meaningless because patients suffering from a gout flair may suprisingly have normal blood levels. However, in patients who are on medications to prevent gout, monitoring the blood uric acid levels can help guide treatment. In addition, hyperuricemia almost always precedes a gout attack.

Signs and Symptoms

As discussed above, the uric acid crystals cause inflammation in the joint space. This leads to a painful, swollen, and red joint. Gout attacks joints asymmetrically, meaning that it rarely affects the same joint on both sides of the body at that same time. Symmetric joint pain is more consistent with other rheumatological diseases.

Many joints can be affected by gout. The most common joint is the metatarsal phalangeal joint (MTP), which is a joint in the big toe. When this joint is involved the disease is referred to as "podagra".

Gout attacks usually occur quickly and unexpectedly with peaking of symptoms within 12 to 24 hours. Multiple repeated attacks of gout can lead to a chronic form of the disease known as "tophaceous gout". In chronic gout, not only are joints affected, but crystal formation can also occur in other areas of the body. For example, the achilles tendon and earlobes can be affected.

Tophaceous Gout

Patients with gout may also be at increased risk of developing uric acid kidney stones due to elevated uric acid in the urine.


Acute treatment is aimed at controlling the inflammatory process within the joint. The most common drugs used to treat acute gout flairs are non-steroidal anti-inflammatory medications (NSAIDSs). Ibuprofen, naproxen, and indomethacin are the most common NSAIDs used to treat gout flairs. Steroids are also sometimes used, especially in people with contraindications to NSAIDs such as kidney failure.

An additional second line medication used to treat acute gout flairs is colchicine. It is typically used in people who cannot tolerate NSAIDs.

To prevent gout attacks from reoccurring, or to prevent tophaceous gout, there are several medicines that are used. The first medication is known as probenecid. It is most effective in people who "under-excrete" uric acid because it inhibits the re-absorption of uric acid in the kidney.

The second medication is known as allopurinol. It is most useful in people who "over-produce" uric acid because it inhibits the enzyme xanthine oxidase (see degradation pathway above) and reduces the amount of uric acid formed from the breakdown of purines.

Allopurinol and probenecid should not be used to treat acute gout flairs. Paradoxically, they can actually worsen an acute flair and should only be used to prevent recurrent attacks.


Gout is a disease of the joints caused by deposition of uric acid crystals. The joint becomes hot, swollen, red, and extremely painful. Diagnosis is made by aspiration of the crystals from the joint space. Treatment for acute flairs is usually with non-steroidal anti-inflammatories. Colchicine is occasionally used as well. Allopurinol and probenecid are used to prevent recurrent attacks.

References and Resources

Burst Fractures: Axial Loading Leading to Ouch!

Burst fractures are a specific type of spine fracture in which the body of a given vertebrae “bursts” into pieces. By definition a burst fracture involves the entire vertebral body. The image below is an example of a normal lumbar spine with the vertebral bodies outlined.

Burst fractures most commonly occur at the junction between the thoracic and lumbar spine. This junction is an area where the rigid thoracic spine transitions to the more mobile lumbar spine, and hence is an intrinsic point of weakness. This is why most burst fractures occur between the T10 through L2 vertebrae.

CT vertebral body

Axial loading of the spine is what causes burst fractures. They typically occur after a traumatic events like car accidents or falls from significant heights. Elderly individuals, and those with poor bone quality, may suffer burst fractures after minor trauma such as falling from a chair.

Signs and Symptoms

Burst fractures invariably present with back pain at the site of the fracture. Depending on the exact location signs and symptoms of nerve root compression or lower spinal cord injury may occur.

If the nerves that dangle in the lumbar spine (aka: the cauda equina) get compressed by the fragments of bone then weakness, numbness, tingling, and even bowel and bladder problems may occur.

Burst fractures between T10 and L1 can cause damage to the end of the spinal cord (the spinal cord ends at L1 or L2 in most individuals), which can lead to lower extremity weakness, or even paralysis, as well as bowel and bladder dysfunction.


Diagnosis of a burst fracture is made using a combination of x-rays, CT scans, and MRIs. These three imaging modalities serve different functions when evaluating the severity of a burst fracture.

X-rays are usually the first imaging ordered in patients with suspected spine fractures. If the plain x-rays show a burst fracture then CT scanning is usually done to further assess the degree of bony injury (see image below for an example of an L2 burst fracture).

MRI is used to detect ligamentous injury. The degree of ligamentous injury indicates a higher degree of instability; information about ligament integrity helps determine treatment options.

Burst Fracture Lumbar Spine


Treatment of burst fractures is highly dependent on the severity of the burst fracture. Treatment is either conservative with immobilization in a brace (ie: a "TLSO" or thoracolumbar sacral orthotic brace) or surgical fixation.

Burst fracture after instrumentation
As a rough rule of thumb patients with any of the following criteria should be strongly considered for surgical correction:

  • Greater than 50% vertebral body height loss.
  • Greater than 25 to 40 degrees of kyphosis.
  • Greater than 50% spinal canal compromise.
  • Significant posterior ligamentous injury.
  • Any neurological signs or symptoms referable to the injury.
  • If the patient fails conservative therapy with a brace.

Surgical correction can be achieved in a variety of ways and is often related to surgeon preference. Some surgeons will remove a significant portion of the fractured vertebral body and place a “cage” in the area, a procedure known as a “corpectomy”. This, combined with rods and screws from posteriorly provides the greatest stability, but has a higher risk of nerve injury. Not uncommonly, the fractured vertebral body is left alone and rods and screws are placed from behind only. This is especially true if the fractured level shows minimal spinal canal compromise.


Burst fractures of the thoracolumbar spine typically occur after high impact axial loading. They usually occur between T10 and L2, but can be seen anywhere in the spine. Patients will almost invariably have pain at the fracture site and may or may not have neurological signs and symptoms depending on the severity of the fracture. Diagnosis is made with CT, plain x-rays, and MRI. Treatment is highly dependent on the individual fracture and ranges from bracing to surgical fixation.

Related Articles

References and Resources

Atlas Fractures: The Weight of the World On Its Shoulders

The atlas, or the first cervical vertebra (C1), is a ring shaped structure. It forms joints with the base of the skull above and the axis (ie: the second cervical vertebrae) below. It also has two foramen transversarium, which are holes that allow the passage of the vertebral arteries on either side of the spinal cord.

Fractures of the atlas occur most commonly with forceful axial loading of the head (ie: a downward force applied to the top of the head). Pressure on the top of the head causes the skull to push down on the atlas, which results in a break(s) of its ring-like structure. Specific fracture types such as a break in the front of the ring, the back of the ring, or one side of the ring versus the other, are dependent on additional force vectors at the time of loading (ie: flexion, extension, lateral bending, etc.).

Fractures of the atlas must also include a discussion of biomechanical stability, which is usually determined by the integrity of the transverse ligament. The transverse ligament attaches the dens (odontoid) of the axis to the anterior ring of the atlas.

Fractures of the atlas with co-existent rupture of the transverse ligament lead to instability of the joint between C1 and C2. In other words, the ring of C1 may be able to move forward relative to the dens of C2. Transverse ligament injury is more common when axial loading is combined with extension of the head.

Not surprisingly, fractures of the atlas often co-exist with fractures of other cervical spine vertebrae. The most common combination is with a fracture of the axis, occurring in up to 40% of cases.

Signs and Symptoms

Patient’s with isolated atlas fractures usually have neck pain and muscle spasms. Frequently they have no injury to the spinal cord because the ring splays outwards as it fractures.

It is important to rule out injuries to the vertebral arteries, which run in bony holes (ie: foramen transversarium) on the sides of the atlas. When injured, the vertebral arteries can cause strokes in the brainstem and cerebellum, which can be life threatening.

Since the atlas is so close to the brainstem, patients may have co-existent injury to the lower cranial nerves. Specifically, injury to the 12th nerve can cause problems with tongue movements, injury to the 11th nerve can cause weakness with shoulder shrug and the ability to turn the head to the side, and injuries to the 9th and 10th cranial nerves can cause problems with swallowing and paralysis of the larynx leading to difficulty with speech.

Co-existent head and brain trauma, which can cause a constellation of different signs and symptoms depending on severity can also occcur.


Diagnosis of an atlas fracture is made using x-rays, CT scans, and MRIs. X-rays should include anterior-posterior views, open mouth odontoid views, and lateral views of the cervical spine. If there is no evidence of neurological injury, flexion-extension x-rays may also be obtained to assess for stability of the C1-C2 joint.

The bony injury associated with atlas fractures is categorized according to the Jefferson or Landell and Van Peteghem classification systems. The Landells classification has three types, whereas the Jefferson classification has four types:

Landell and Van Peteghem Classification
Type 1 Fracture of either the anterior or posterior ring, but not both (posterior ring fractures are most common type)
Type 2 Fractures of both the anterior and posterior ring
Type 3 Fracture of the lateral mass(es)

Jefferson Classification
Type 1 Fracture of the posterior ring only
Type 2 Fracture of the anterior ring only
Type 3 Fracture of the anterior and posterior rings on both sides; this is the classic "burst", or traditional “Jefferson” fracture
Type 4 Fracture of the lateral mass(es)

Atlas fracture

An important part of diagnosing atlas fractures involves assessing the integrity of the transverse ligament, which is best done using MRI. However, if an MRI cannot be performed then open mouth odontoid, flexion-extension x-rays, and CT scans can provide some information regarding transverse ligament injury.

The rule of Spence is one way of assessing the integrity of the transverse ligament on an open mouth odontoid x-ray. The rule states that if the right and left lateral masses of C1 overhang the lateral masses of C2 by greater than a total distance of 6.9mm than the likelihood of co-existent transverse ligament injury is high. The rule of Spence is not fool proof and should be supplemented with MRI and/or flexion-extension films whenever possible.

Atlantodental Interval
Another method for assessing transverse ligament injury is using the "atlantodental" interval (see image to the left). This is the distance between the anterior arch of C1 and the odontoid process (aka: dens) of C2.

This interval is usually quite small, typically less than 3mm in adults and 5mm in children. If the interval is greater than this, then co-existent transverse ligament injury should be suspected.


Treatment of isolated atlas fractures is usually with cervical immobilization. This may be with a halo or with a rigid cervical collar such as a cervical-occipital-mandibular-immobilizer (SOMI).

Atlas fractures that have co-existent transverse ligament rupture often require an operation to stablize the bones of the spine. This is usually in the form of fusing the atlas or occiput (back of the head) to the second cervical vertebrae.

If other injuries (ie: fractures of C2) are present and/or there is significant ligamentous injury then open surgical fusion of the bones may be necessary to re-create stability of the craniocervical junction.


Atlas fractures occur in response to vertical compression of the head on the upper cervical spine. Fractures of the anterior, posterior, or both rings of C1 may be present. Biomechanical stability is typically determined by assessing the integrity of the transverse ligament. Patients with isolated C1 fractures usually complain of neck pain, and rarely have injury to the spinal cord. Diagnosis is based on CT, x-ray, and MRI findings. Treatment is with rigid external immobilization or operative spinal fusion.

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Hodgkin’s Lymphoma: B-Cells, Pel-Ebstein, and EBV

Lymphoma is a cancer that develops from cells in the body known as lymphocytes. Lymphocytes are a subcategory of white blood cells, which are the cells that help ward off infection. There are two different types of lymphocytes: B-cells and T-cells. The majority of lymphomas, including Hodgkin’s disease, stem from B-cells.

In Hodgkin’s disease a B-cell, for unknown reasons, becomes cancerous. The cell then makes many clones of itself. These cells bundle together to form a solid tumor known as a lymphoma.

Why B-cells in Hodgkin’s lymphoma become cancerous is not entirely known. One belief is that infection with Epstein-Barr virus (the same virus that causes infectious mononucleosis) can cause the cells to turn cancerous in genetically susceptible people. Other theories are that certain genetic translocations may be the underlying factor. As of yet, no particular theory has significant supporting data to call it the true cause. It is likely that the development of Hodgkin’s disease is multi-factorial.


Reed-Sternberg Cell

There are different types of Hodgkin’s lymphoma. They are based on unique histopathological (ie: what it looks like under a microscope) characteristics, and are important in determining prognosis.

The histopathological features the pathologist looks for are the number of Reed-Sternberg cells, as well as the number of lymphocytes present in the biopsy specimen. A Reed-Sternberg cell is a funny shaped cell with two nuclei that looks like an "owl’s eyes" (see image to the right). They are believed to form when two cells merge together under the influence of certain proteins produced by the Epstein-Barr virus.

The first category, and most common type, is nodular sclerosing Hodgkin’s lymphoma. In this type, there are very few Reed-Sternberg cells with a moderate number of lymphocytes. It commonly occurs in younger individuals, and with treatment, the prognosis is excellent.

The second category is mixed cellularity Hodgkin’s lymphoma. This type has many Reed-Sternberg cells, and a moderate number of lymphocytes when viewed under the microscope. It has an intermediate prognosis.

The third category is lymphocyte predominant Hodgkin’s. It has very few Reed-Sternberg cells and many lymphocytes. It occurs most commonly in males less than 35 years of age. It is also one of the few types that is not associated with Epstein-Barr virus infection.

The last category is lymphocyte depleted. It is the rarest form of Hodgkin’s lymphoma. It typically affects older males.

Hodgkin's Types
Unfortunately it has the worst prognosis of the four types types.

The image to the left is one way of organizing the different Hodgkin’s types and their prognosis based on age, number of RS cells, and prognosis. LP = lymphocyte predominant, NS = nodular sclerosing, MC = mixed cellularity, LD = lymphocyte depleted.

Signs and Symptoms

The classic presentation of Hodgkin’s lymphoma is painless enlargement of the lymph nodes. This is similar to non-Hodgkin’s lymphoma, and the only way to differentiate the two is through biopsy.

Systemic manifestations may occur and include night sweats, fever, and weight loss. However, these are more common in patients with disseminated (ie: metastatic) disease. Interestingly, a pathognomonic (ie: seen exclusively in Hodgkin’s lymphoma) feature that occurs in some cases is pain of the involved nodes after drinking alcohol. Finally, a symptom known as Pel-Ebstein fevers are also specific for the disease. A Pel-Ebstein fever is a cyclical fever that occurs for several weeks at a time followed by a fever free period.

Other signs related to the immune system can be seen in patients with Hodgkin’s lymphoma. A condition known as cutaneous anergy can occur. Anergy refers to a lack of response by the cell mediated immune system. For example, in patients with tuberculosis a reaction will occur underneath the skin when they get a TB test. This reaction is the result of their cell mediated immunity reacting to the tuberculosis components injected underneath the skin. However, in anergic patients no reaction is seen, even if they have tuberculosis! This can also occur in patients with Hodgkin’s disease.


Hodgkin's Disease PET-CT
Diagnosis of Hodgkin’s lymphoma is made by looking at a biopsy specimen underneath the microscope. The most common way of obtaining a specimen is through biopsy of a lymph node. Differentiating Hodgkin’s from other types of lymphomas is important because it determines the best treatment options.

Additional studies are often performed to determine the number and location of involved lymph nodes. One such study is a positron emission tomograph (PET) combined with a CT scan. Any lymph nodes involved "light up" on the scan. An example, with the arrows pointing to involved nodes, is shown to the right.


Staging of Hodgkin’s lymphoma was traditionally based on a system known as the Ann Arbor Classification. It is divided into four stages. In stage 1 disease a single lymph node, or single organ is involved. In stage 2 disease involvement of multiple (two or more) lymph node regions on the same side of the diaphragm is present. In stage 3 disease involvement of nodes on both sides of the diaphragm is present; the spleen or other limited organ involvement may also be present. In stage 4 disease multiple organs are involved; interestingly, lymph node involvement is not necessary for a stage 4 diagnosis, although it is commonly present. Finally, each stage is further divided into “A” and “B” depending on whether or not symptoms are present. If symptoms are present, the stage is upgraded to a “B”.

Ann Arbor Classification (simplified)
Stage 1 Single lymph node or organ
Stage 2 Multiple lymph nodes on same side of diaphragm
Stage 3 Lymph nodes on both sides of diaphragm
Stage 4 Multiple organs involved

However, more recently the Lugano staging classification has become the preferred method. It divides disease into limited and advanced. Limited disease includes stage 1 and stage 2. Stage 1 involves a single lymph node or nearby nodes. Stage 2 involves two or more nodal groups. Advanced disease includes stages 3 and 4. In stage 3 disease nodes on both sides of the diaphragm are involved as is the spleen. Stage 4 disease is disseminated disease into organs. There are sub-categories in the Lugano model as well.


Like most cancers treatment is highly dependent on the stage of the disease. In most cases chemotherapy and radiation are used. Radiation is directed at involved lymph nodes, as well as lymph nodes that are uninvolved, but nearby. Common chemotherapeutic agents used include: adriamycin, bleomycin, vinblastine, vincristine, prednisone, procarbazine, and mechlorethamine.


Hodgkin’s lymphoma is a cancer of a type of white blood cell known as a B-cell. There are numerous categories depending on its histopathological characteristics. Patients often have painless enlarged lymph nodes. Some patients have fever, weight loss, and other non-specific symptoms. Staging is based on the Ann-Arbor model. Treatment usually involves a combination of chemotherapy and radiation.

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