Testicular Torsion - Medcomic

Testicular torsion occurs when the spermatic cord (from which the testicle is suspended) twists, cutting off the testicle's blood supply, a condition called ischemia. The principal symptom is rapid onset of testicular pain. The most common underlying cause is a congenital malformation known as a "bell-clapper deformity" wherein the testis is inadequately affixed to the scrotum allowing it to move freely on its axis and susceptible to induced twisting of the cord and its vessels.
Testicular torsion usually presents with sudden, severe, testicular pain and tenderness involving one testicle. There is often nausea and vomiting due to the pain.

Some of the symptoms are similar to epididymitis though epididymitis may be characterized by discoloration and swelling of the testis, often with fever, while the cremasteric reflex is not affected. Testicular torsion, or more probably impending testicular infarction, can also produce a low-grade fever.

Pathophysiology

Torsion is due to a mechanical twisting process. It is also believed that torsion occurring during fetal development can lead to so-called neonatal torsion or vanishing testis, and is one of the causes of an infant being born with monorchism (one testicle).

Intermittent testicular torsion

A variant is a less serious but chronic condition called intermittent testicular torsion (ITT), characterized by the symptoms of torsion but followed by eventual spontaneous detortion and resolution of pain. Nausea or vomiting may also occur. Though less pressing, such individuals are at significant risk of complete torsion and possible subsequent orchiectomy and the recommended treatment is elective bilateralorchiopexy. Ninety-seven percent of patients who undergo such surgery experience complete relief from their symptoms.

Extravaginal testicular torsion

A torsion which occurs outside of the tunica vaginalis, when the testis and gubernaculum can rotate freely, is termed an extravaginal testicular torsion. This type occurs exclusively in newborns. Neonates experiencing such a torsion present with scrotal swelling, discoloration, and a firm, painless mass in the scrotum. Such testes are usually necrotic from birth and must be removed surgically.

Torsion of the testicular appendix

This type of torsion is the most common cause of acute scrotal pain in boys ages 7–14. Its appearance is similar to that of testicular torsion but the onset of pain is more gradual. Palpation reveals a small firm nodule on the upper portion of the testis which displays a characteristic "blue dot sign." This is the appendix of the testis which has become discolored and is noticeably blue through the skin. Unlike other torsions, however, the cremasteric reflex is still active. Typical treatment involves the use of over-the-counter analgesics and the condition resolves within 2–3 days.

Treatment

With prompt diagnosis and treatment the testicle can often be saved. Typically, when a torsion takes place, the surface of the testicle has rotated towards the midline of the body. Non-surgical correction can sometimes be accomplished by manually rotating the testicle in the opposite direction (i.e., outward, towards the thigh); if this is initially unsuccessful, a forced manual rotation in the other direction may correct the problem. The success rate of manual detorsion is not known with confidence.

Testicular torsion is a surgical emergency that requires immediate intervention to restore the flow of blood. If treated either manually or surgically within six hours, there is a high chance (approx. 90%) of preserving the testicle. At 12 hours the rate decreases to 50%; at 24 hours it drops to 10%, and after 24 hours the rate of preservation approaches 0. About 40% of cases results in loss of the testicle. Common treatment for children is surgically sewing the testicle to the scrotum to prevent future cases.

Epidemiology

Torsion is most frequent among adolescents with about 65% of cases presenting between 12 – 18 years of age. It occurs in about 1 in 4,000 to 1 per 25,000 males per year before 25 years of age; but it can occur at any age, including infancy.

Instinctive drowning response

 
The instinctive drowning response is a set of behaviors automatically undertaken by a person who either is, or is very close to, drowning. These are autonomic responses of the body, undertaken without deliberate control, and "represent a person's final attempts to avoid actual or perceived suffocation in water" before sinking.

Contrary to the normal popularisation of drowning as a highly visible behavior, involving shouting, abrupt or violent movements such as splashing and waving, and visible difficulty—which is a related phenomenon, known as aquatic distress, which often but not always precedes drowning—the "instinctive drowning response" is noiseless and confined to subtle movements.

 Description

While distress and panic may sometimes take place beforehand, drowning itself is deceptively quick and often silent. A person at, or close to, the point of drowning is unable to keep their mouth above water long enough to breathe properly and is unable to shout. Lacking air, their body cannot perform the voluntary efforts involved in waving or seeking attention. Involuntary actions operated by the autonomic nervous system involve lateral flapping or paddling with the arms to press them down into the water in the effort to raise the mouth long enough to breathe, and tilting the head back. As an instinctive reaction, this is not consciously mediated nor under conscious control. The lack of leg movement, upright position, inability to talk or keep the mouth consistently above water, and (upon attempting to reach the victim) the absence of expected rescue-directed actions, are evidence of the condition.

Timing

The instinct takes place for typically no longer than the final 20–60 seconds during drowning and before sinking underwater.In comparison, a person who can still shout and keep their mouth constantly above water may be in distress, but is not in immediate danger of drowning compared to a person unable to do so.

Recognizing drowning

To an untrained observer, it may not be obvious that a drowning person is in distress—they may appear to be swimming safely while within 20–60 seconds of sinking under the surface. Drowning victims generally show no visible panic in their movements, because they quickly become incapable of making noticeable gestures or calling for help. They cannot kick their feet, nor swim to a rescuer, nor grasp a rope or other rescue equipment. They may be misunderstood as "playing in the water" by those unfamiliar with drowning, and other swimmers just meters away may not realize that an emergency is occurring. Lifeguards and other persons trained in rescue learn to recognize drowning people by watching for these instinctive actions.

In emergency situations in which lifeguards or other trained personnel are not present, it is advisable to wait for the victim to stop moving or sink before approaching, rescuing, and attempting to resuscitate. While the instinctive reaction to drowning is taking place, victims latch onto any and all solid objects in attempts for air, which can result in the drowning of a would be rescuer as well as the victim.

The event called 'AVIR Syndrome' (Aquatic Victim Instead of Rescuer) has killed over 100 would be rescuers in Australia and over 80 would be rescuers in New Zealand. In Australia, 86 of these rescuers who drowned were trying to rescue children and they had failed to follow basic rescue safety rules that are easily learned.

 Research and discovery

The common drowning behaviors were identified by Frank Pia based upon study of video footage of actual and near-drownings, and documented in his 1971 instructional video On Drowning, and a 1974 paper[9] Observations on the drowning of nonswimmers.

At the time, it was commonly believed that drowning involved agitated behaviors, although Pia cites an earlier (unspecified) 1966 paper as also observing this was not necessarily the case.

Lung Volumes and Capacities - MedComic.com

The following terms describe the various lung (respiratory) volumes:

• The tidal volume (TV), about 500 mL, is the amount of air inspired during normal, relaxed breathing.

• The inspiratory reserve volume (IRV), about 3,100 mL, is the additional air that can be forcibly inhaled after the inspiration of a normal tidal volume.

• The expiratory reserve volume (ERV), about 1,200 mL, is the additional air that can be forcibly exhaled after the expiration of a normal tidal volume.

• Residual volume (RV), about 1,200 mL, is the volume of air still remaining in the lungs after the expiratory reserve volume is exhaled.

Summing specific lung volumes produces the following lung capacities:

• The total lung capacity (TLC), about 6,000 mL, is the maximum amount of air that can fill the lungs (TLC = TV + IRV + ERV + RV).

• The vital capacity (VC), about 4,800 mL, is the total amount of air that can be expired after fully inhaling (VC = TV + IRV + ERV = approximately 80 percent TLC). The value varies according to age and body size.

• The inspiratory capacity (IC), about 3,600 mL, is the maximum amount of air that can be inspired (IC = TV + IRV).

• The functional residual capacity (FRC), about 2,400 mL, is the amount of air remaining in the lungs after a normal expiration (FRC = RV + ERV).

Some of the air in the lungs does not participate in gas exchange. Such air is located in the anatomical dead space within bronchi and bronchioles—that is, outside the alveoli.

Cardiac Conduction - MedComic.com

Introduction:

The cardiac conduction system is responsible for the organized transmission of electrical impulses in the heart. This system consists of a network of cells that transmits electrical potentials from the atria to the ventricles.

The Conduction Circuit:

The sinoatrial node, which is located in the right atrium, is responsible for the generation of electrical impulses. These impulses are then transmitted through atrial conduction tissue to the atrioventricular node. The atrioventricular node causes a slight delay in transmission, and then allows the signals to travel to the cells of the interventricular septum. The conduction fibers in the interventricular septum are known as the bundle of His. These fibers divide into the left and right bundle branches, which transmit electrical impulses to the left and right ventricles, respectively.

Properties of the Conduction System:

The ability of the conduction system to stimulate the heart to contract in an organized fashion stems from its intrinsic properties. These properties include: excitability, conductivity, and automaticity.

-Excitability: Refers to the ability of a cell to respond to an electrical stimulus.

-Conductivity: Refers to the ability of each cell of the conduction system to conduct individual electrical impulses from one cell to another.

-Automaticity: Refers to an individual cell’s ability to “self-excite” without any impulse from an outside source.

The conductive tissue that has the fastest automaticity acts as the pacemaker of the heart. In a normal heart, the sinoatrial node has the highest automaticity and, thus, acts as the primary pacemaker of the heart. However, if one pacemaker in the heart fails to act, the conduction tissue with the next fastest rate will gain control of the pacing function. Each component of the conductive system has its own intrinsic rate of self-excitation, as follows:

-The sinoatrial node has an intrinsic rate of 60-100 beats per minute.

-The atrioventricular node has an intrinsic rate of 40-60 beats per minute.

-The ventricular conduction tracts have an intrinsic rate of 15-40 beats per minute.

The spontaneous generation of cardiac electrical signals, as well as their propagation, is due to alterations in electrolyte concentrations. The major electrolytes that are involved in this process include: Sodium, Calcium, Potassium, Magnesium, and Chloride.

Sodium:

Sodium plays a vital role in automaticity, which is a property characterized by the heart’s ability to generate spontaneous, repetitive contraction stimuli.

Calcium:

Calcium is also essential for automaticity and, in addition, plays a vital role in cardiac contractions.

Potassium:

Potassium’s role in the heart is to reset the repetitive firing system so that it can quickly become active after each electrical stimulus it generates.

Magnesium and Chloride:

The roles of Magnesium and Chloride are unclear, but low levels of these electrolytes impair the replacement and functioning of Sodium, Calcium, and Potassium, thus altering overall heart activity.

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When Is It Too Late To Call A Trauma Activation?

When Is It Too Late To Call A Trauma Activation?

Admit it. It’s happened to you. You get paged to a trauma activation, hustle on down to the ED, and get dressed. The patient is calmly and comfortably lying on a cart, staring at you like you’re from Mars. Then you hear the story. He has a grade V spleen injury. But he just got back from CT scan. And his car crash wasyesterday! 

Is this appropriate? The answer is no! But, as you will see, the answer is not always as obvious as this example. The top thing to keep in mind in triggering a trauma activation appropriately is the reason behind having them in the first place.

The entire purpose of a trauma activation is speed. The assumption must be that your patient is dying and you have to (quickly) prove that they are not. It’s the null hypothesis of trauma.

Trauma teams are designed with certain common features:

• A group of people with a common purpose
• The ability to speed through the exam and bedside procedures via division of labor
• Rapid access to diagnostic studies, like CT scan
• Availability of blood products, if needed
• Immediate access to an OR, if needed
• Recognition in key departments throughout the hospital that a patient may need resources quickly

Every trauma center has trauma activation triage criteria that try to predict which patients will need this kind of speed. Does the patient in the example above need this? NO! He’s already been selected out to do well. Why, he’s practically finished the nonoperative solid organ management protocol on his own at home.

Here are some general rules:

• If the patient meets any of your physiologic and/or anatomic criteria, they are or can be sick. Trigger immediately, regardless of how much time has passed.
• If they meet only mechanism criteria and it’s been more than 6 hourssince the event, they probably do not need the fast track.
• If they only meet the "clinician / EMS judgment" criteria, think about what the suspected injuries are based on a quick history and brief exam. Once again, if more than 6 hours have passed and there are no physiologic disturbances, the time for needing a trauma activation is probably past.

If you do decide not to trigger an activation in one of these cases, please let your trauma administrative team (trauma medical director, trauma program manager) know as soon as possible. This may appear to be undertriage as they analyze the admission, and it’s important for them to know the reasoning behind your choice so they can accurately document under- and over-triage.

From: http://regionstraumapro.com/

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