Case Presentation 1


NAME: Quincy Questionable         DOB: 9/26/1975                      SEX: Male

RACE: Hispanic                          PHYSICIAN: Victor Joe, MD     DATE: 12/02/2010

CHIEF COMPLAINT: Crush injury to bilateral lower extremity

HISTORY OF PRESENT ILLNESS: 35 year old Hispanic male who was brought in by the ambulance after he tripped and fell into an industrial press at work. Both of the patient’s legs were crushed while in the trash compactor. His fellow employees had pulled him out of the industrial press before EMS arrived on scene. There is obvious deformity, ecchymosis and swelling. The patient is awake and alert and states he is unable to feel both of his legs and also unable to move his legs, toes, or feet. There was no loss of consciousness at any time. The patient arrived on a backboard with a cervical collar, which were both cleared to be taken off shortly after his arrival. The patient was hypotensive in the field and was given approximately 500 cc of 0.9 % normal saline in the field prior to arrival. Upon arrival to the ED the patient’s airway was patent, he was breathing room air spontaneously and had a normal skin color and temperature. He was speaking coherently and his Glascow Coma Score was 15. He was Spanish speaking only, so a translator was used.


PAST MEDICAL HISTORY: none per wife and sister-in-law.

ALLERGIES: none per wife and sister-in-law.

MEDICATIONS: none per wife and sister-in-law.

SURGERIES/HOSPITALIZATIONS: none per wife and sister-in-law.

SOCIAL HISTORY: Denies tobacco use, alcohol use and drug use, per wife and sister-in-law. Patient lives at home with his wife who is 6 months pregnant and 10 year old son. Works as an Insulation Contractor


FAMILY MEDICAL HISTORY: unable to obtain.

REVIEW OF SYSTEMS: unable to obtain because patient was in extreme pain upon arrival. 


  • Vital Signs: P 132 R 22 T 95.6 BP 107/76 SpO2: 97% on room air
  • General: alert and oriented x3, in extreme pain.
  • HEENT: Head-normocephalic, atraumatic; Eyes- PERRLA, EOM-intact, conjunctiva clear, no scleral icterus. Ears- intact, no discharge; Nose- patent, no discharge; No facial lesions or trauma.
  • Skin: warm and dry, no cyanosis or pallor except bilateral lower extremities. Bilateral lower extremities- + pallor, ecchymosis, and swelling. Stab wound to bilateral upper thigh.
  • NECK: trachea midline, no adenopathy, full ROM, no JVD.
  • CHEST: stable, equal rise and fall, no retractions, no instability or crepitus.
  • LUNGS: clear to auscultation bilaterally, no wheeze, rhonchi or rales, no pericardial friction rub, normal respiratory effort.
  • CVS: Tachycardic, regular rhythm, no murmurs, rubs, or gallops. 2+ radial pulses bilaterally, 0+ femoral, posterior tibial and dorsalis pedis pulses bilaterally. + edema in bilateral lower extremities.
  • Abdomen: soft, non-distended, non-tender, bowel sounds present and normoactive in all 4 quadrants, no organomegally, masses, or guarding.
  • GU: pelvis stable.
  • Extremities: obvious deformity to bilateral femur/upper thigh. No palpable femoral, dorsal pedal, or posterior tibial pulse. Feet are cold with delayed capillary refill. No movement or sensation in bilateral lower extremities. + edema in bilateral lower extremity.
  • Spine/Back: no step-off’s, no obvious trauma.
  • Neuro: Cranial nerves II-XII grossly intact. Mental status: alert and oriented x 3. Reflexes: 0+ left patellar (L4), 0+ right patellar (L4), 2+ right brachioradialis (C6), 2+ right triceps (C7) and biceps (C5). Motor function: decreased strength on LLE and RLE (0/5 strength). Normal strength of RUE and LUE (5/5). No atrophy, hypertrophy or fasiculations. Sensory function: no light touch, pain, proprioception or 2 point discrimination of bilateral lower extremities. GCS 15.



Workup in ER:

  • Chemistry (BMP)
    • K: 5.1, Na: 145, Cl: 121, CO2: 17, BUN: 12, Cr: 0.6, Glucose: 133, Ca: 5.6, Phos: 3.9, Mg: 1.1.
  • Hematology
    • WBC: 3.5, Hgb: 8.6, Hct: 25.2, Plt: 37
  • CPK-465
  • Lactate
  • CT of abdomen: no injury
  • CT of pelvis: multiple fractures involving pubic rami, left acetabulum, left sacrum, L5 vertebral body, left lamina, left L4 transverse process, bilateral communited proximal femur fracture , bilateral superficial femoral artery occlusions.
  • CT angiogram bilateral LE: vascular compromise
  • CXR(supine):
  • X-Ray(RLE and LLE): bilateral femur fracture



1.) Open bilateral lower extremity femur fracture

2.) Bilateral vascular and nerve injury

3.) hypothermia



  • ER management:
    • 4L 0.9% NS
    • heart monitor
    • O2- via non-rebreather at 10L/min
    • Zofran 4 mg IV
    • Fentanyl 25 mg IV (x2)
    • Ancef 2 gm IV
    • Transfuse 2 Units PRBC
    • Insert foley catheter to monitor output
    • Warming blankets/lights
    • Ortho consult
    • Send to OR immediately
  • OR management:
    • Intra-medullary nailing of bilateral femurs
    • Left above the knee amputation
    • Right re-vascularization (femoral-femoral bypass with autologous popliteal vein from left leg).
    • decompressive laparotomy for abdominal compartment syndrome
    • Fasciotomy right lower extremity for compartment syndrome
    • 20 units PRBC transfused
  • Post-Op management:
    • Ventilation support
    • Hemodynamic monitoring, fluid resuscitation
    • Monitor for rhabdomyolysis
    • Ortho consult
    • Neuro checks on RLE- plan for staged AKA of right LE in OR






            Fractures occur by 2 different mechanisms: either to little mechanical stress on a bone causes it to weaken and break or on the other hand, to much mechanical stress on a bone also causes it to break. A pathologic fracture is one that results from disease that weakens the bone locally, so that a fracture occurs with normal stress. Elderly are at the greatest risk for pathologic fractures.

There are also several different types of fractures. A single fracture line is called a simple fracture. A simple fracture that extends all the way through the bone is a complete fracture and one that does not is considered incomplete. Multiple fractures at a single site are considered a comminuted fracture. A greenstick fracture is one that occurs most commonly in children because their bones are more flexible and tend to bend or break partially. An impacted or compression fracture is one in which sudden end to end force causes a bone to collapse on itself. Twisting force can cause a spiral fracture. A stress fracture is one that occurs slowly after repeated microfractures caused by high stress.

The femur bone is a strong bone with an excellent blood supply. Femoral shaft fractures are most common in children and previously had a mortality rate of 50% mainly because the treatment approach was inadequate. With an advancement in the treatment of femoral shaft fractures from prolonged bed rest to plating and intra-medullary rods there has been a decrease in mortality associated with these types of fractures. The femoral shaft extends from 5 cm distal to the lesser trochanter to 6 cm proximal to the adductor tubercle. There are three types of fractures of the femoral shaft, each with a different treatment approach. These include: spiral, transverse, or oblique shaft fractures, comminuted femoral shaft fractures and open femoral shaft fractures. Comminuted fractures are further classified by Winquist based on the size of the fracture fragment and the degree of comminution. Most femoral shaft fractures are closed; open fractures often result from compounding from within.

In 75 % of cases, femoral shaft fractures are caused by a high-energy force in the form of either a direct blow or an indirect force transmitted though a flexed knee. The most common cause is a motor vehicle accident, but gunshot wounds represent growing number of femoral shaft fractures as well. In children, a fall from a significant height and child abuse must be suspected.

A patient presenting with a femoral shaft fracture will be in severe pain and visible deformities will likely be present. Hemorrhage and formation of a hematoma are likely and will cause the thigh to be swollen and tense. The involved extremity may also be shortened and there may be associated crepitus with movement of the leg. Extensive soft-tissue damage, bleeding and shock are also commonly associated with femoral shaft fractures. Thus, associated injuries of the sciatic nerve and superficial femoral artery and vein should also be assessed. A neurologic exam should be performed to rule out sciatic nerve involvement, the thigh should be assessed for expanding hematoma and dorsal pedal and posterior popliteal pulses should be palpated to assess for associated arterial injury. Displacement of the fracture is usually attributed to the surrounding musculature. A fracture of the proximal 1/3 of the femur bone is generally abducted, flexed, and externally rotated. This position is due to the gluteal muscles that insert on the greater trochanter and abduct the proximal segment, while the iliopsoas muscle that inserts on the lesser trochanter externally rotates and flexes the proximal segment. A midshaft fracture undergoes a varus deformity because of the pull of the medial adductors on the distal fragment and the pull of the lateral muscles on the proximal fragment. A fracture of the distal 1/3 of the femur bone is generally angulated anteriorly due to the force applied by the gastrocnemius muscle.

In order to correctly diagnose a fracture of the femoral shaft, routine AP and lateral X-rays are generally adequate to visualize the fracture. However, hip and knee views should be included as there is often associated injury in these areas as well.

Due to the severe forces required to produce a fracture of the femoral shaft, there are often several other injuries that accompany the fracture. These include, other ipsilateral fractures, dislocations, and ligamentous injuries of the hip and knee. Ipsilateral femoral neck fractures are found to occur in 6% of patients with femoral shaft fractures. Bleeding is also a major concern associated with femoral shaft fractures. The femur has a rich blood supply and thus, the average blood loss from a femoral shaft fracture is 1-1.5 L. However, bleeding just into the thigh in a closed femoral fracture is not sufficient to produce hypotension, so in patients with a femur fracture and hypotension, other causes of bleeding must be sought. Associated injuries of the sciatic nerve are uncommon (2%) with a femoral shaft fracture due to the protective quality of the surrounding musculature.

Treatment of a traumatic femoral shaft fracture varies depending on the age of the patient and the location of the fracture, but it generally includes immobilization of the affected extremity in a traction splint or pneumatic anti-shock garment. Traction splints provide immobilization, distract the fragment and provide less space for bleeding and a decreased incidence of hypotension. However, if an associated injury of the sciatic nerve is suspected, the traction splint should be substituted with a plaster splint to avoid further nerve injury. Pain medication should be administered, as well as blood and fluids. Closed treatment of a femoral shaft fracture is an option mainly for pediatric patients. Closed treatment consists of immobilizing the extremity in a hip spica cast or traction for 3-6 weeks, until the fracture is “sticky” enough for spica casting. Acceptable alignment with this procedure is difficult to obtain in an adult and the prolonged recumbany required can result in complications like DVT and pressure ulcers. The definitive treatment of femoral shaft fractures is closed intra-medullary nailing, if done early this allows early mobilization of the patient and prevention of fat embolism. It also allows for better alignment and improved knee and hip function by decreasing the time spent in traction. Intra-medullary fixation is generally performed closed rather than open, which decreases the chance of infection by decreasing the amount of soft tissue dissection needed.. Comminuted fractures can also be treated with intramedullary nailing as long as screws are used to fix both the proximal and distal bone segments to the nail to avoid shortening and malrotation of the fracture. The treatment of open femoral fractures is slightly more complex, requiring emergent operative debridement. The healing rate of femoral shaft fractures is generally high and approaches 100% after closed nailing techniques.

In a recent study, it has been shown that early stabilization of pathological bilateral femoral fractures by intra-medullary nailing is associated with increased mortality rate. The study compared the mortality of patients with unilateral femur fractures to those with bilateral femur fractures and concluded that only 11.7% with unilateral fractures died, while 25.9% of those with bilateral fractures died. It was found that this difference was due more to the severity of other injuries associated with bilateral femur fractures than the fractures themselves, indicating that physicians should be more concerned with diagnosing and treating additional problems in patients with bilateral femur fractures than attempting to perform immediate intra-medullary nailing of the femur fracture. However, because patients with bilateral femur fractures present with higher injury severity score and higher degrees of trauma, this itself may be the cause of higher complication rates and not the order of the treatment itself. It was also found that primary femoral stabilization by intra-medullary nailing increases the inflammatory response, which occurs in addition to that induced by the initial trauma. If this response is intense enough it may tip a borderline stable multi-trauma patient toward decompensation. The release of inflammatory mediators, surgical blood loss, and hypothermia can over-stimulate the host immune system. Through a well described interactions’ pathway of activated inflammatory molecules the end result might be endothelial damage and remote organ failure. These findings have led to the current practice of damage control orthopedics over immediate intra-medullary nailing for treatment of bilateral femur fractures due to the risk of higher complications with immediate intra-medullary nailing.

Several complications of femoral shaft fractures exist and include: nonunion, malunion, delayed union or infection, malrotation of the extremity, breakage of nails and plates used to fix the fracture, arterial injury with delayed thrombosis or aneurysm formation, peroneal nerve injury, and thigh compartment syndrome. Compartment syndrome is caused by increased pressure in closed osteofascial spaces which compromises circulation and perfusion of the tissues in the involved compartment. Nerves and muscle tissue are most susceptible to this decrease in perfusion. Fasciotomies are performed through the skin and fascia to decrease the pressure within the compartment. The wounds are left open dressed and treated by delayed primary closure. If treatment of compartment syndrome is delayed for as little as 6-8 hours it can lead to irreversible nerve and muscle damage.



Skinner, Harry B. . Current Diagnosis & Treatment in Orthopedics. New York: Lange             Medical, 2003. Print.

Simon, Robert R., Scott C. Sherman, and Steven J. Koenigsknecht. Emergency

            Orthopedics: the Extremities. New York: McGraw-Hill, Medical Pub. Division,

  1. Print.

Stavlas, Panagiotis, and Peter V. Giannoudis. “Bilateral Femoral Fractures: Does

Intramedullary Nailing Increase Systemic Complications and Mortality

Rates?” Web of Science. Nov. 2009. Web. 07 Dec. 2010.


A fib treatments


Treatment Options for atrial fibrillation:


  1. Electrical Cardioversion-
  • patients that are hemodynamically unstable (low blood pressure or heart rate) and need immediate rate control.
  • Patients with persistent afib (must be anticoagulated with coumadin for 4 weeks before cardioversion to prevent an embolus from traveling to the brain and causing a stroke).
  1. Pharmacologic Cardioversion with Anti-arrhythmic medications (amiodarone, dofetilide, ibutilide, propafenone, flecainide):
  • Patients with recurrent paroxysmal or persistent atrial fibrillation
  1. Rate control and anticoagulation
  • Rate control- beat blockers, calcium channel blockers, occasionally digoxin used alone or in combination.
  • Anticoagulation- coumadin. Use CHADS2 score described earlier to determine who needs coumadin.
  1. Catheter ablation
  2. Surgical ablation


*2 trials compared the results of rate control and anticoagulation (treatment option 3 above) with normal sinus rhythm control (treatment option 2 above) and found that there was no higher rate of death or stroke in the rate control than the anticoagulation group.


*Elective cardioversion is generally recommended for the initial episode of atrial fibrillation in patients in whom it is thought to be of recent onset and when there is an identifiable precipitating factor. Cardioversion is also appropriate in patients who remain symptomatic. However, the recurrence rate is sufficiently high enough that long term anticoagulation with warfarin should be continued until NSR can be proven to exist for 6 months straight.


* Elective cardioversion can be achieved either electrically or pharmacologically (using the anti-arrhythmic medications listed above.


*Unfortunately, sinus rhythm will persist in only 25% of patients who have sustained (lasting more than several days) or recurrent episode of atrial fibrillation. However, if the patient is treated long-term with an anti-arrhythmic medication, sinus rhythm will persist in about 50%.

As you can see there is much to know about atrial fibrillation. I hope that you found my review helpful and if you are in medicine, you’ve learned a couple things. If you liked what you read, feel free to leave a comment below!



Afib Part 2

The Electrical Conduction System:

Cardiac muscle has 2 unique properties that predispose it to arrhythmias: automaticity and gap junction transmission. Cardiac smooth muscle cells, unlike skeletal muscle cells, exhibit spontaneous depolarization and are able to transmit electrical signals from one cell to another via gap junctions. This property is beneficial because it allows the heart to depolarize and propagate the electrical impulse without the need for central nervous system initiation.

The interiors of myocytes or heart muscle cells are negative or “polarized” at rest. The release of free calcium (Ca2+) ions into the interior of the myocytes causes the interior of the cell to become positive or “depolarized” and stimulates them to contract. The cell-to-cell conduction of depolarization through the myocardium is carried by fast-moving sodium (Na+1) ions. Repolarization is the electrical phenomenon that occurs immediately after depolarization, when the interiors of the myocytes once again become negative due to outflow of potassium (K+) ions from the myocytes. Repolarization occurs so that the myocytes can recover their resting negative charge and be depolarized again.

The SA (sinoatrial) node is the hearts dominant pacemaker and its pacing activity is known as “sinus rhythm”. It initiates a wave of depolarization that spreads outward, stimulating the atria to contract. It is located in the upper posterior wall of the right atrium and initiates depolarization in regular intervals. Each depolarization wave generated by the SA node spreads through both atria and appears as a p-wave on the EKG. The p-wave represents atrial depolarization and contraction. This simultaneous contraction of the atria forces the blood they contain to pass through the AV valves (mitral and tricuspid) into the ventricles. These AV valves (tricuspid and mitral) prevent the backflow of blood into the atria from the ventricles and electrically insulate the atria from the ventricles, leaving the AV node as the sole conduction pathway between the atria and ventricles. The AV node is just above and continuous with a specialized conduction system that distributes depolarization to the ventricles very efficiently. When the wave of depolarization enters the AV node, depolarization slows, producing a brief pause and allowing time for the blood in the atria to enter into the ventricles. This slow conduction through the AV node is carried by calcium ions. After the wave of depolarization is conducted through the AV node, it shoots rapidly through the ventricular conducting system beginning with the HIS bundle and right and left bundle branches which are bundles of rapidly conducting “purkinje fibers” that spread out just beneath the endocardium and directly depolarize ventricular myocytes. Depolarization of the ventricles produces a QRS complex on the EKG.

Atrial fibrillation is considered to be a reentry arrhythmia or a disorder of impulse transmission. Reentry requires at least 2 conduction pathways with a variable block in one of the pathways. If the 2 pathways for conduction have similar conduction velocities (speeds), the electrical impulses will merge distally (downstream) and no arrhythmia will occur. If an event (premature atrial contraction, etc) occurs at the right time to make on the these 2 conduction pathways refractory (still depolarized or positive, not repolarized or negative), the impulse will be blocked in that pathway and not able to travel through. Meanwhile, the electrical impulse that traveled down the other conduction pathway, may continue back up the previously refractory pathway, which is now repolarized and ready to conduct and the arrhythmia will sustain itself.

Phew! that is a ton of high tech mumbo jumbo right? Especial for people in Scranton, PA.

Rest assure, the next couple are a little toned down…



Hope you’re liking everything…

As you can see, I love medicine and have no trouble talking about anything and everything related to the human body. There will be more to come about atrial fibrillation as it is highly important and one of the main causes of stroke in the united states. The others being carotid disease and hypertension, or high blood pressure. Keep in mind, I am trying to keep this website fun yet informative. There is literally so much to learn about medicine and no possible way you can know everything about everything. Anyway. I hope you’re having a good time checking out my site! see you next time.



Lets Talk About A-fib

Background of Atrial Fibrillation:

Atrial fibrillation is the most common chronic arrhythmia (irregular heart rhythm) with an incidence and prevalence that increase with age, affecting 10% of people over 80. It may occur alone or concomitantly with other forms of heart disease that cause enlargement of the atira (valvular heart disease, dilated cardiomyopthay, arial septal defect, hypertension, and coronary artery disease). It may be the initial presenting sign in thyrotoxicosis (hyperthyroidism). Conditions such as pericarditis, chest trauma, cardiac surgery, thyroid disorders, and pulmonary disease may predispose a patient to afib. Acute alcohol withdrawl or alcohol excess may also precipitate afib. I am covering this topic because my father had suffered a stroke caused by a fib while working on his roof. Click here to check his business.


The way I think about afib is that any disease that will cause an enlargment of the atria of the heart will predispode a patient to atrial fibrillation. For some reason, the larger the atria, the more likely it is that afib will occur. Valvular heart disease causes atrial enlargement because if a valve is stenotic (stiff and doesn’t open as easily or as widely as it should), it causes blood to back up into the atria. The larger the volume of blood in the atria, the more the walls will stretch (like filling a balloon with water). The other cardiac disease listed above cause the same problem by different means. I will explain this more tomorrow if you have questions. The enlargement of the atria along with the irregularity of the heart rhythm results in more blood pooling in the atria and remaining there, unable to be fully ejected into the ventricles. Virchow’s triad describes the 3 characteristics that are thought to lead to thrombosis or clotting of the blood. The 2 characteristics are blood STASIS (or pooling), hypercoaguability, and vessel injury. Clearly in afib, there is blood stasis and when blood is just “hanging around” and not moving, it is more likely to form blood clots or thrombi. Theses clots are then floating around the atria and free to leave the heart through the aorta and travel through the carotid arteries up to the smaller blood vessels in the brain and block them. When this occurs, part of the brain is starved of blood supply and thus oxygen, we know all tissues need oxygen to survive, so without oxygen, part of the brain dies. This is what a stroke is. 


The heart rhythm in atrial fibrillation is always irregular, but the ventricular rate may range from slow to fast. The EKG demonstrates erratic, disorganized atrial activity between discrete QRS complexes (signify ventricular depolarization and contraction) that occur in an irregular pattern. Atrial fibrillation often occurs paroxysmally (transiently) before becoming the established rhythm.


The are three types of atrial fibrillation presentations: first is paroxysmal atrial fibrialltion which means simply that the atrial fibrillation comes and goes on its own, without the assistance of antiarrhythmic drugs or cardioversion to convert the patient out of atrial fibrillation. Second is persistent atrial fibrillation, this generally means that the patient needs antiarrhythmis drugs, cardioversion or surgical ablation to convert them out of atrial fibrillation. Lastly, there is permanent atrial fibrillation, which is usually treated with “rate control and rat poison” meaning that we attempt to control the heart rate with a beta blocker thus reducing the patient symptoms and we use coumadin, an antocoagulant to reduce the risk of thrombus or clot formation in the left atrium and subsequent embolization or “travel” to the blood vessels of the brain causing a stroke.


There are also three types of atrial fibrillation electrically speaking, first is atrial fibrillation rate controlled, meaning that the venricular response is controlled or between 60-100 beats per minute. Second is atrial fibrillation with a slow ventricular response, meaning that the ventricular response or heart rate is less that 60 beats per minute. Lastly is atrial firbrillation with a fast ventricular response, meaning that the ventricular response or heart rate is over 100 beats per minute.


Up to 2/3 of patients with a first episode atrial fibrillation will convert back to sinus rhythm spontaneously in 24 hours. If atrial fibrillation persists for longer than a week, it is unlikely to spontaneously revert to sinus rhythm and will require some type of treatment or intervention.

The most serious consequence of atrial fibrillation is thrombus formation and subsequent embolization of the thrombus to the cerebral circulation, causing a CVA (cerebrovascular accident or stroke) or TIA (transient ischemic attack). The “CHADS2” score is used to determine what patients would benefit from anticoagulation with COUMADIN. CHADS2 is an acronym that stands for C-congestive heart failure, H-hypertension (high blood pressure), A-age >75, D-diabetes, S-stroke gets 2 points. One point is assigned for each condition that the patient has, except that stroke gets 2 points. If the total points are over 2, the patient will most likely benefit from therapy with coumadin which will reduce the risk of thombus (clot) formation in the left atrium and this embolization (movement) of the thrombus to the cerebral circulation.