Microsurgery in Podiatry

MICROSURGERY is intricate surgery performed using miniaturized instruments and a magnifying instrument, preferably portable such as a variant of Loupes, or a fixed microscope.
In podiatry, such microsurgery is indicated in repair of nerve entrapment, microvasculature repair, and skin-muscle-tendon grafting or repair.
Typically, deep neurovasculature travels together: comitante vein, artery, and nerve. Proper anatomy identification plays a major role in differentiating artery from vein. A surgeon can use several methods, one being the simplest by blocking vasculature flow to the area in question and slowly releasing the flow observing which structure fills back: first artery fills up, then vein in retrograde fashion. This leaves out the nerve.
In a nerve entrapment, scared tissue extends along its tract sometimes strangulating surrounding tissue.
In my future practice and procedures, I will seek an instant identification of nerve structure from surrounding tissue. A simple chemical marker, yet non-reactive to surrounding tissue is in demand. Its application should vary from being injected or simply applied directly in a sterile wash from a dispensing syringe.
The function of the marker is to perform the following: quickly embed within the epineurium of the questionable nerve structure, and become easily visible either by itself or under a specific visible light spectrum, i.e. UV. It is important to realize this nerve identification is non-reactive to surrounding tissue including epineurium. Once the nerve tissue is identified by the protein marker, it is freed from surrounding tissue using microsurgery, and to prevent further scaring, a layer of regenerated tissue matrix is applied along the nerve sheath.
Typically the scar surrounding the nerve is made primarily of collagen fibers, extracellular proteins with triple helical structures making up the fibrillar and microfibrillar network of extracellular matrix. When nerve ending is damaged, the normal extracellular matrix synthesis is up-regulated. It turns out this hinders the regeneration of new nerve sprouts to reach new interface(s). With microsurgery, new avenues of nerve entrapment repair are possible. Currently there is no one single successful procedure. The use of protein epineurium marker as adjuvant procedure should help the successful identification of healthy nerve tissue from surrounding extracellular matrix allowing successful repair without unnecessary damage to healthy nerve tissue.

Made of Stardust

STAR-gazing, such a privilege to ascend into the past of hundreds of million of years ago as projected into our eyes by long lived photon energy.

stargazer |ˈstärˌgāzər|noun informal an astronomer or astrologer.• a daydreamer.

I feel it is far too seldom we find ourselves looking up into the nakedness of the sky above us. I feel we do ourselves a great disservice ignoring our origins.

Late Carl Sagan used to say "We are all made of stardust", billion year old carbon. I can't explain the peace I feel each stargaze I embrace. But I look around and see so many of us busy with lives and the living, and forgetting of the past we used to admire. Up there hangs our dreams, our pasts, and ultimately our future. Stargazing is to some a place of retreat, but always one of comeback.

From the beginning of time, we have always looked up in to the sky to seek comfort or closure from the unknown. In the end, looking up should produce a feeling of both awe and unmatched realization of our puny little existence, the devout symbol of humanity in the face of infinite infinitesimal.

Nicotine Blows, Literature Review

BACKGROUND
Nicotine has intrigued me to the point where I decided to investigate it. I've come across many articles and references realizing how far we have come to understanding its intricate mechanisms on physiologic and cellular levels. This is only but a notably brief summary of my lengthy research on Nicotine smoking and its deleterious effects to human body.


A quick search leads to basic facts about Nicotine: first ever records point to French-Portugal trade in 1500's, when seeds of Nicotiana tabacum plant became a trading contributor. Since then, it has been used in recreation, medicine, and as insecticide. By 1900's lung cancer was linked to tobacco smoking. Then its side effects started to be taken seriously as they involved every single aspect of the body, including psychiatric, skin health, soft tissue, blood vessels, dentition, hair loss, and not to mention every single major organ of the body. Not soon enough, it was realized that Nicotine smoking was the most efficient drug delivery system.


Because Nicotine has a very short half-life in serum, meaning it lasts in its active form for few minutes while in the blood stream, the smoker continues to dose frequently, which is at the core of the addiction. And with frequency, comes desensitization, thus with time the smoker is seeking increased concentration of Nicotine to reach the same high.


I briefly mentioned Nicotine use as insecticide, which is formulated at very high concentrations. If ingested, however, this causes death within minutes secondary to asphyxiation due to respiratory failure (paralysis).



FACTOIDS
-Nicotine from inhaled tobacco reaches the brain between 5-10 seconds.
-Inhaled smoke gets you 90% of Nicotine in bloodstream.
-Only 20-50% of it gets in your blood from smoke taken into mouth and exhaled.
-Nicotine use remains the leading preventable cause of death in the world.



VASCULATURE EFFECTS
Chronic Nicotine exposure causes long-term homeostatic regulation of endogenous nicotinic acetylcholine receptors (short named nAChRs), which plays a key role in adaptive cellular processes, thus leading to addiction.

In another words, smoking causes a up-regulation of nicotinic acetylcholine receptors, especially of the specific heteromeric receptors non-Alpha7-nAChRs, which by exclusion factor is the Beta2-nAChRs.


You may ask, where are these receptors mainly located? Through tests and imaging studies, these up-regulation of receptors take place in lateral septum, caudate putamen, and nucleus accumbens, or in another words, somewhere inside the brain. Naturally, it is there that our Nicotine seeking takes place, however Nicotine receptors are found throughout our body in every tissue explaining why the effects are so wide spread. [1]


In another study, it was noted that smoking caused a sharp increase in blood pressure and heart rate. Despite this, there was no notable change in stroke and systemic vascular resistance. Interestingly, smoking caused increase in extremities blood flow, primarily in the muscle and a decrease in blood flow to the skin. This study also showed that in habitual smoker, an increase heart rate was observed.


Why is this important to know? Direct effect of smoking causes short term increase in arterial wall stiffness, which is harmful to artery itself, increasing the risk of plaque rupture. Acute cardiovascular events are mainly due to plaque rupture. This shows that smoking (each time you light up that cigarette) might heavily contribute to acute ischemic events. [2]


Yet another study talks about the increased aortic systolic blood pressure and increased arterial stiffness. They call to attention reduced pulse pressure amplification and increased arterial wave reflection, all due to adverse hemodynamic effects. All this means blood flow is adversely decreased in extremities primarily the skin. [3]



WHAT IS COTININE?
You may ask, how can a physician tests a patient if previous smoking occurred? It is done by measuring serum cotinine concentrations. A study reviewed serum cotinine acceptable levels, with low levels between 0.2-1.6ng/mL, and the high of above 1.7ng/mL. This procedure is useful when assessing tobacco exposure in children, known as second hand smoking effects. As explained in this study, children with medium to high levels of serum cotinine showed an increase in aortic Young’s elastic modulus and a decrease in aortic distensibility. This report shows a direct relationship between passive smoking and arterial elasticity in children. [4]


All these previous reviewed studies talk about macrovasculature, i.e. aortic and carotid vessels. Instead, let’s continue by looking at microvasculature, typically those seen in the heart coronary arterial tree, and peripheral microvasculature. The effects of one hour of exposure to tobacco smoke showed a significant decrease in late rise in skin blood flow in response to heating. One way to stimulate the skin’s microvasculature is by directly heating it, which normally should lead to localized vasodilatation and increased localized blood flow. However, this test showed a delayed response of skin to directly warming it, concluding microvasculature was, for lack of better words "in trouble". [5]



KEY POINTS 
Thus far, we can partially conclude that tobacco smoking specifically increase the macrovasculature (aortic wave reflection) through Nicotine-dependent pathway, and impairs microvasculature function, even past the end of the exposure of Nicotine. In another words the afore mentioned nicotinic effects last for at least minutes to hours after you threw away that finished cigarette. Recalling a previously mentioned fact, while the Nicotine half-life is extremely short, its effects last for relatively long time.


But how is the microvasculature impaired? In a study, researchers concluded that Nicotine directly increases the Norepinephrine NE receptors in the skin capillaries, thus producing vasoconstriction. Do you recall the previously mentioned study where heating up the skin produce vasodilatation? Well, another means to produce similar effect is by use of Nitroglycerine NTG, which is a potent vasorelaxant.


In practice, patients requiring skin incisions, skin flap reconstruction, amputations, and other skin procedures, all will experience a tremendous delay in healing time including complications such as rejection of skin grafts secondary to local vascular spasm and subsequent localized ischemia. Poor vascular flow leads to delayed or blocked delivery of nutrients and removal of normal cellular waste, an important attribute to healing. [8]



PREGNANCY EFFECTS
I've always wondered what were the typical effects seen in pregnant women who smoke Nicotine. Several studies investigated such effect. One in particular has shown that smoking caused an acute decrease in intervillous placental blood flow, which had an apparent normalization within 15 minutes. What is expected with decrease blood flow to placenta, even if momentarily? Answer is, direct growth retardation of fetus and other complications of pregnancy including stillborns, premature infants, and low birth weight. [6]





LUNG EFFECTS
Besides lung cancer, what ever happens with those smokers who have the typical chronic nagging cough? It turns out that these individuals have an increase lung tissue concentration of macrophages primarily, increased presence of endothelial adhesion molecules, and cytokines. All these inflammatory cellular conglomerate produce symptoms typically seen in non-smokers who are diagnosed with chronic bronchitis.

The bad news is, smokers who decide to quit are expected to continue experiencing these chronic bronchitis symptoms from weeks to months in a row. However, over time respiratory symptoms will decrease dramatically and so will the nagging bronchitis. The good news is overall lung respiratory capacity will improve with time, as seen in greater than 12 months Nicotine free individuals. [7]



CAUSE & EFFECT
Risk factors are everywhere. Annals of Internal Medicine defines it in a 1961 article as "something that increases the chance of getting a disease or infection." This however does not take into consideration subclinical comorbidities and subclinical symptoms. A disease becomes apparent when it is symptomatic and negatively interferes with individual's daily life activities. [9]


In brief, Nicotine is known by many as a major risk factor for many disorders, including cancer, respiratory disease, heart disease, diabetes, stroke, and peripheral arterial or venous insufficiency. This research has in part shown me that the presence of other comorbidities significantly increase the complication rate and speed by which known diseases become symptomatic in nicotinic abusive population.


What does this mean for the patient and the medical team carrying for such patients? It significantly eliminate treatment options, increases the length of recovery, chance of infection, and life expectancy. This in turn makes living difficult for patient and those who care for them, making them harder to comply to medical regiment imposed by medical team. Expectantly, non-compliance is experienced by many patients caught in this tug war of delayed healing time, the outcome being more complications, more interventions, and the cycle repeats to no avail.



References:
1. Long-term effects of chronic Nicotine exposure on brain nicotinic receptors, Morgane Besson, et al., PNAS 2007
2. Short and long-term effects of smoking on arterial wall properties in habitual smokers, Mirian J.F. Kool et al, JACC 1993
3. Effect of Smoking on Arterial Stiffness and Pulse Pressure Amplification, Azra Mahmud, et al, JAHA 2002
4. Decreased Aortic Elasticity in Healthy 11-Year-Old Children Exposed to Tobacco Smoke, Katariina Kallio, et al, JAAP 2008
5. Acute Effects of Passive Smoking on Peripheral Vascular Function, Jean-François Argacha, et al, JAHA 2007
6. The Acute Effects of Smoking on Intervillous Blood Flow of the Placenta, P. Lehtovirta, et al, BJOG 2005
7. Effect of smoking cessation on airway inflammation in chronic bronchitis, G Turato, et al. JRCCM 1995
8. Effect of Nicotine on vasoconstrictor and vasodilator responses in human skin vasculature, Claire E. Black, et al, JRICP 2001
9. The Framingham Offspring Study, H. J. C. Swan, et al, JACC 1999

The Difficult Tetanus - Case Presentation: A lesson learned.

This blog post is different than my previous. As a medical student on rotations, I am constantly faced with a wide variety of events, some more dramatic than others. In the process, I research current literature and methods of treatment. The following is a recent encounter with a patient infected with tetanus. From history, I soon discover that despite being recently immunized with a booster shot, patient continued to display the classic presentation of tetanus, which unfortunately turned for the worse. In her remembrance and for a better cause, I put together a review on tetanus and what you have to know to prevent its infection. Know what you should do to prevent its manifestations. The story begins with a review.

 

If you thought you were immunized, think again...

Tetanus is an acute often fatal Nervous System (NS) disorder characterized by SUSTAINED muscle spasms and convulsions caused by the toxin-producing anaerobe CLOSTRIDIUM TETANI, which is a obligate anaerobe Gram+ Bacilli (exotoxin), typically found in soil. 

Its clinical features and presentation associated with traumatic injuries have been well-known before the introduction of tetanus toxoid vaccination in 1940’s (among ancient Greeks and Egyptians).

This is the only vaccine preventible disease that is infectious but not contagious between humans.

Keep in mind that the typical bacteria forms a terminal spore that is resistant to heat and antiseptics. However, the organism outside the spore is very sensitive to Oxygen and heat. Another thing to keep in mind is  the very low concentration of toxin needed - minimal lethal dose is 2.5 nanograms/Kg.

Clostridium Tetani usually enters the body through a deep penetrating wound. In presence of anaerobic conditions, typically seen with a local inflammation or early infection, the spores germinate, which later produce the bacteria and the toxin, disseminated via blood and lymphatics.

Toxin acts at certain CNS locations: peripheral motor end-plates, spinal cord, brain, and sympathetic nervous system. Toxin interferes with release of neurotransmitters, blocking inhibitor impulses, which leads to unopposed muscle contraction, and autonomic NS may also be affected.

Once Clinical manifestation occurs after tetanus reached the presynaptic inhibitory nerves, there is little that can be done to slow down disease progression. 
In assessing prognosis, generally the shorter the incubation the worse the outcome.

Incidence and mortality from tetanus by age group in the United States, 1998–2000. (From Pascual FB, et al: Tetanus surveillance—United States, 1998–2000. MMWR Surveill Summ 52[SS-3]:1, 2003.)

Despite the availability of an effective vaccine, tetanus remains endemic worldwide. It is more common in warm, damp climates and relatively rare in cold regions. The global incidence of tetanus is estimated to be between 800,000 and 1 million cases a year, with half occurring in neonates.

Since the introduction of vaccination programs in the United States, the incidence of tetanus has steadily declined from 4 cases per million population in the 1940s to 0.095 cases per million population in 2005.

The highest incidences occurs in people older than 60 years (0.35 cases per million population), Hispanic Americans (0.37 cases per million population), and diabetics (0.70 cases per million population). Fifteen percent of cases occur in injection drug users. The overall case fatality rate is 18% but approaches 50% in patients older than 70 years. Cases have been reported in patients who had been fully vaccinated, but in the eight patients from 1998 to 2000, no deaths occurred.

Clinical Diagnosis: Trismus

trismus |ˈtrizməs|nounMedicinespasm of the jaw muscles, causing the mouth to remain tightly closed, typically as a symptom of tetanus. Also called lockjaw.ORIGIN late 17th cent.: from modern Latin, from Greek trismos ‘a scream, grinding.’

Cultures (anaerobes, time consuming, takes minimum three days to get results back; half the time, the results are false negative because of the difficulty localizing and culturing the bacilli). 

Differentials: 

• Strychnine Poisoning Dystonic reactions to Dopamine Antagonist drugs 
• Oropharyngeal infection (DDX Cephalic Tetanus) 
• Hypocalcemia (DDX Neonatal Tetanus) 
• Meningoencephalitis (DDX Neonatal Tetanus).

The goal of immunization is to provide a continuous serum concentration of 0.01 IU/mL of neutralizing antitoxin. Protection between levels of 0.01 and 1.0 IU/mL is not absolute; some authorities consider an antibody level of 0.15 IU/mL or greater as protective.

Active Immunization is achieved via the Tetanus Toxoid (takes time to build immunity).

Passive Immunization is achieved via the Immune Globulin TIG (passive transfer of active immunoglobulins).

Immunization is given immediately if the patient's tetanus immunization history is not available or is uncertain, or if 60 months or more have elapsed since the last booster dose (5 years or more). TIG is given for other than minor wounds if the number of immunization doses the patient received is fewer than three or is unknown. The antibodies neutralize only free toxins, toxin not bound to nerve.

Table 1. Example of management pre-exposure, typically seen in pediatric patients:

Primary and Secondary Immunization.

 

Table 2. Example of management post-exposure:

 The four treatment strategies for patients with tetanus should be undertaken simultaneously: 
(1) aggressive supportive care, control of muscle spasm with Benzodiazepines - most IV benzos except midazolam have propylene glycol as a coingredient which at high doses causes Lactic Acidosis. But midazolam has a short half life. 
(2) elimination of unbound TS (tetanospasmin), with HTIG or TIG (passive immunization)
(3) active immunization, and 
(4) prevention of further toxin production - treating the C.tetani infection via wound debridement and ABX metronidazole.

Metronidazole - antibacterial, antiprotozoal, microbicidal, against most obligate anaerobics and protozoa, interferes with DNA/ Cytotoxic.

Penicillin - antibacterial, blocks cell wall synthesis, against gram+ bacteria and spirochetes.

Tetracycline - protein synthesis inhibition, bacteriostatic against both Gram+ and Gram -.

 

CASE PRESENTATION:

Chief Complaint (CC): This is the case of an 86yo female status-post (s/p) 1 day inability to open mouth, s/p 6 days rusty metal puncture wound Right Lower Extremity RLE.

NLDOCATS*: Patient (PT) complaints of generalized dull aching pain with a scale of 8-9/10 (0 no pain, 10 worst pain) to leg, neck, and abdomen. Pt relates to a 6 (SIX) days old puncture wound to lower extremity (LE) from a rusty metal soft tissue traumatic encounter. Pt relates to onset of fever and chills several days after her initial injury (day zero) for which she has taken Cipro orally prescribed by her primary care physician (PCP) over the phone. Pt relates, her fever resolved uneventfully. However, pt states few days later after taking Cipro orally, she was awaken to discover her inability to open mouth more than a few millimeters, along with increased stiffness to the neck muscles throughout the morning hours. In patient's defense, a confirmed recent Tetanus booster was completed mid-September 2011, prescribed by her PCP.

(*Nature, Location, Duration, Onset, Course, Aggravating factors, Treatment, Special)

Past medical, surgical, and social histories are non contributory. 

Pt allergies are as follows: Aspirin, Penicillin, Sulfa, Ceclor, Mefoxin, Tetracycline, Nalidixic Acid (Neggram), all producing asthma-like reaction. 

Current Medications: Prednisone 10mg QOD
, Theophylline 100mg daily, 
Beclomethasone spray QID
, Albuterol MDI 2 puffs QID
, Imodium PRN, 
Primidone 50mg at bed time
, Fish Oil
, MVI, 
Vit-C, Ca, Vit-D.

Review of Systems: (ROS) Abdominal pain, Diffuse muscle stiffness, Puncture wound RLE with surrounding erythema, Bruising, ELSE remainder of ROS is non contributory

Physical Exam:
 

Vital Signs: T 96.8, HR 85, RR 16, BP 150/78, PO2 
99% room air
. 

General: Awake Alert and Oriented to person, place, & time (AAOx3), Emaciated, Restless 


HEENT: Atraumatic, Normocephalic Anicteric, External ocular movements intact, pupils equally round reactive to light and accommodation (PERRLA), Unable to open jaw > 0.5cm, mucous membrane moist, teeth worn


Neck: Post cervical neck muscles are spastic, tender
, 

Cardiovascular: regular rate and rhythm (RRR), no murmurs, gallops, rubs, S3, S4, no peripheral edema

Respiratory: clear to auscultation (CTA) bilaterally (BIL), no wheezing, crackles


Abdomen: normative bowel sounds (BS), abdomen firm to palpation, unable to determine hepatoslenomegaly given muscle rigidity


Extremities: UE Strength 5/5 BIL, epicritic sensation intact in all 4 extremities, LE Strength 4/5 BIL, R-Knee Extension 2/5, Dorsal Plantar flexion 5/5 BIL. There is 1-1.5cm circular area of necrosis on Lat LE with fresh tissue in middle that is leaking clear fluid, surrounding erythema cold to palpation, nontender to palpation. 

Neurologic: Cranial nerves II-XII intact, when asked to smile patient exhibited sardonic smile, baseline tremor in BIL hands. Muscle strength as described above. Sensation intact to all 4 extremities


Psychiatric: AAOx3, fluent speech pattern, thoughts are logical, judgement and insight appear to be fair.

Laboratories: CBC & BMP are within normal limits


Podiatry Physical Exam:
 LE exam reveal several scabs and a wound on the L anterior leg. There are bandages, which are dry and intact and remain in place over this area. Left leg shows no erythema, edema, or heat. Pedal Pulses are palpable. Right leg exhibits significant erythema from the level of the mid calf distally. There is +1 pitting edema throughout the lower leg and foot. Pedal pulses palpable, however faint secondary to edema which is present. There is a dry bandage covering the wound located to the R lateral lower leg midtibia level. Examination of wound reveals a black eschar approximately 2cm diameter. Wound borders appear intact with notable erythema, edema, and heat throughout surrounding area. Noted induration palpable proximally and posteriorly to the wound, extending 3cm posteriorly. Upon compression of periwound area there is noted purulent fluid drainage from wound. Patient also responds and is sensitive to this palpation, attempting to retract leg.

Assessment & Plan: 


1. Trismus with generalized spasticity consistent with Tetany. Give a total of 3000 Units IG. Start Metronidazole 500mg Q6H. Cardiac Monitoring. IV Fluids and Valium 2mg every 6h for muscle spasms. Also Magnesium sulfate IV 40mg/kg, or Labetalol IV 0.25-1.0mg per minute for autonomic dysfunction. 

2. Nutrition, emaciated, NG tube or PEG placement for expected 4-6 weeks long tetany course

Podiatry Surgical Debridement: 

Upon Examination, wound appeared erythematous with central eschar. Sharp debridement performed of all devitalized soft tissue, minimal purulence observed for which aerobic / anaerobic cultures were performed. Skin appeared atrophic dissecting easily along the superficial and deep fascial planes proximally. Mechanical Pulse-Lavage performed with 3000 mL Triple Antibiotic in sterile Normal Saline. Wound was packed open and sterile soft dressing applied. Patient transported to Recovery in stable condition, no complications observed. 

Summary of Events:

Day 0: Injury 

Day 4: Fever 100F, Sweats. Tx Cipro PO at home 

Day 5: Symptoms resolve 

Day 6: Locked Jaw, Stiff Neck, RLQ Pain, RLE Pain
➡ ED admission, Intubation, Tetanus IG 3000 IU, Metronidazole 500mg IV Q6H, Valium, IV fluids, Magnesium IV, Labetalol IV. 

Day 7: Sx Wound Debridement w/ Pulse Lavage

Day 10: Severe generalized deterioration, Cardiovascular Instability, not responding to treatment, Autonomic NS failure, possibly Phrenic Nerve involvement. 

Day 12: Immediate family disconnects life support, Pt expires within minutes.

RESOURCE - Tetanus Algorithm:

 

REFERENCES

1. C. Louise Thwaites,  Lam Minh Yen, Harrison's Principles of

Internal Medicine, 18e, Infectious Diseases > Section 5. Diseases Caused by Gram-Positive Bacteria > Chapter 140. Tetanus, McGraw-Hill Companies 2012

 

2. Madonna Fernández-Frackelton, Infectious Diseases - Bacteria, Rosen's Emergency Medicine 7th Ed 2010

 

3. Itzhak Brook, Etiologic Agents of Infectious Diseases - Tetanus, Principles and practice of Pediatric Infections 3rd Ed, Churchill Livingstone, An Imprint of Elsevier, 2009

 

4. Pavani Reddy, Thomas P. Bleck, Clostridium tetani (Tetanus) 244, Bleck, Mandell, Douglas, & Bennett's Principles and Practice of Infectious Diseases, 7th ed - Textbook of Critical Care , Sixth Edition, 2009 - Churchill Livingstone, An Imprint of Elsevier

 

5. C. Louise Thwaites, Lam M. Yen, Tetanus 147, Bleck, Mandell, Douglas, & Bennett's Principles and Practice of Infectious Diseases, 7th ed - Textbook of Critical Care , Sixth Edition, 2009 - Churchill Livingstone, An Imprint of Elsevier

 

6. Gregory J. Moran et al, Antimicrobial Prophylaxis for Wounds and Procedures in the Emergency Department, Journal of Infectious Disease Clinics of North America, 22 (2008) 117–143

 

7. Basic Tetanus Algorithm, AJM PRiSM 2009

 

A LEARNING LESSON:

• if you suspect a dirty tetanus prone infection/deep skin cut
• flush the wound with clean water by placing the wound under running water, removing visible dirt, debris, or foreign materials; I recommend prying open the sound if it's large enough to ensure water flushing is maximized. 
• do not apply sodium peroxide as this strong base will start the local inflammatory process secondary to complete cellular destruction, especially host skin and soft tissue; applying an antibiotic ointment is also not recommended since you need to keep the wound clean and dry for the time being. 
• recall, tetanus spores do not like oxygen & dry environment
• apply a clean gauze / dressing over the affected area and have someone drive you to the nearest Emergency Department. The sterile gauze is the best method to keep the wound as dry as possible absorbing any serous or blood discharge from the wound preventing anaerobic environment. 
• an injection of Immune Globulin is highly indicated despite your history of tetanus booster shots. Tetanus Immune Globulin (TIG) is the only known neutralizer of free unbound tetanus toxin that will soon be released from within the wound. 
• a treatment of oral Metronidazole antibiotic (anti anaerobe gram positive bugs) is highly recommended to treat local soft tissue infection that might reverse the wound to an anaerobic environment.
• recall, the tetanus spore will germinate and release the bacilli into the wound as soon as the wound becomes anaerobic environment seen with early inflammation and infection. Once bacilli is aware of anaerobic environment it will quickly release its toxin which will travel via lymphatics and blood vessels selectively to nerves of muscle, spinal cord, and brain. Once toxin is bound to the nerve it will not be unbound until the nerve end-plate regrows a working duplicate bud that will replace the damaged end-plate - an approximate 4-6 weeks period. 

 

 

American Rag

Traveling, anywhere, an antidote to boredom or the seed for resilience. Sometimes I travel because I feel the need to be away from the epicenter. Other times, I am chased out of my comfort zone. A mode of survival, I guess.

In life's adventure, I will never be too sure who will play the most influence. Not until that formidable influence were gone forever from my embrace, only realize that after the fact. Is that a socio-psychologic effect, one of self fulfilling prophecy?

When I was a young child, I often looked at my elders with interest and distance. There were some questions in my mind that I suppressed for the longest time. But as I too become one of them, I can feel the answer settling in. Every single one of us, will always stay young at heart, despite the aging body, the ship in which we must coexist. It is a sad metaphor, but there is no such thing as aging self.

It is a typical turn of evens that over the years we normally turn to other problems that govern our lives, and as a side effect we will loose the curious child that brought us where we are. Have I lost him yet? When we realize we lost it the question remains, what will we do about that? I know I will try to seek him back every chance i have. But is that feasible? In our progressive process, a new comfortable self has long been established. That core value will not change unless, a direct threat to our existence is imminent. Anything can tip that balance. And we're never ready for it when it happens.

I often pretend to understand the intricate workings of life and death, but pretend is all I do, for I will never truly understand. Medical student or not, the basics are all out there for everyone to grasp. And yet, sometimes there are no answers to seek. Just acceptance. Can you imagine a world with no answers? I can't.

NoAgendaShow dead? Not so fast Citizens!

Taking the http://www.noagendashow.com/ to a new level

I appreciate the efforts people pull from across "le globe" with weekly donations to support "the best podcast in the world!"

However, I often wondered the simplicity of this system. And there is no surprise "for reasons more than one" the public donations are drying up. How long can this last for what is worth? I want to believe it will last for as long as Adam and John can hang in there, sane enough to deconstruct the media and "watch CSPAN so we don't have to."

In the morning to you all, to all ships at sea, boots on the ground, and feet in the air, moon bases, cooks in the kitchen, and drones in the air, and of course the rest of human resources

It is time to introduce new things to the show to take it to a new level:

1. New voices. Let's introduce new voices, such as Micky, Adam's uncle, or Andrew Horowitz.

2. Shuffle the show's structure around. Don't be so rigid. It may be fun to have the birthdays shout-out early on and knighthood later. Be inventive.

3. Let the finances transparency begin. Build a system that shows a financial goal set for each show, updated every hour, so the rest of "human resources" know how much is needed to keep the "dough rolling."

Money is what keeps the world turning. But just as money is important to you, Adam and John, it is important to me, and everyone else. In my opinion the show needs a financial system such that it will keep a steady substantial cash flow going for years ahead, a system that is self perpetual. I believe the current free-will pure-donation system governing the noagendashow causes frustration not only to the hosts but also to its listeners.

As an example, set a financial goal for each show, lets say $2,500. Then, let users know how much of the goal is fulfilled, an hourly auto refresh would be necessary. Despite of the impressive number of users each episode, the responsibility to pay forward is spread thin, a typical thing seen in a large group of people where only a few pay large amounts of money. Could limiting the number of executive producers per show help fulfill a steady flow from the rest of users who want participate but feel pushed aside? Let's face it, the greater majority of people are cheap, so if there were so much ambiguity about how much is needed per show, the full potential of the financial pipeline is not fully utilized.

Build it and it will come.

So what happens if the goal set forth per show were reached, and a producer wants to give some love from paypal or the bank? At that point, it is entirely up to that producer whether to continue with donation or keep the money for the next show. In addition, it could be possible for any producer to pay in advance for one or two shows ahead. This ensures a steady flow and everyone is happy.