Monday, November 21, 2011

CIRCUMCISION MADE EASY


DORSAL SLIT METHOD OF CIRCUMCISION

The dorsal slit method requires more surgical skill than the forcepsguided
method. It is helpful to have an assistant present during the
procedure, although it can be done without one. There is a risk that
more skin is cut away from one side than the other, giving an
asymmetric result. Nevertheless, the technique is widely used by
general and urological surgeons throughout the world. It is the
technique illustrated in the WHO manual, Surgical care at the district
hospital.1

Step 1. Prepare skin, drape and administer anaesthesia, as described
above.

Step 2. Retract the foreskin and remove any adhesions, as described
above.

Step 3. Mark the intended line of the incision, as described above.

Step 4 (optional). Some surgeons prefer to mark the line of incision
by making a very shallow incision using a scalpel. This is useful on a
deeply pigmented man on whom it is difficult to see the line of the
marking pen or dabs of gentian violet. Before making the shallow
incision, check carefully that the incision line is level with the corona
and that even amounts of skin are marked for removal from each side
of the penis. The incision should be made just through the skin; it is
very important not to cut too deeply and divide blood vessels (Fig.
5.27).

One disadvantage of marking the line of incision with a scalpel is that
there may be an increased risk of accidental injury to the surgical staff.
In addition, a relatively inexperienced surgeon may cut too deeply.
However, these risks must be balanced against the risk of a poor result
of the circumcision operation if the marking is difficult to see and too
much or uneven amounts of skin are removed.


Step 5. Grasp the foreskin with artery forceps at the 3 o’clock and 9
o’clock positions. Take care to apply the artery forceps so that there is
equal tension on the inner and outer aspects of the foreskin.



Step 6. Place two artery forceps on the foreskin in the 11 o’clock and 1
o’clock positions (Fig. 5.29). Check that the inside blades of the two
artery forceps are lying between the glans and foreskin, and have not
been inadvertently passed up the urethral meatus.



Step 7. Between the two artery forceps, in the 12 o’clock position, use
dissection scissors to make a cut (the dorsal slit) up to the previously
marked incision line (Fig. 5.30).




Step 8. Using dissection scissors, cut the foreskin free, following the
previously marked circumcision line (Fig. 5.31).




Step 9. Any skin tags on the inner edge of the foreskin can be
trimmed to leave approximately 5 mm of skin proximal to the corona
(Fig. 5.32). Care must be taken to trim only the skin and not to cut
deeper tissue.



Step 10. Stop any bleeding and suture, as described in steps 7–10 of
the forceps-guided method.

Step 11. Check for bleeding. If there is none, apply a dressing (see
“Dressing” at the end of this chapter).


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Sunday, November 20, 2011

Dorsal penis block



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ECG-Myocardial Infarction

Source: ABC of ECG (BMJ)


Hyperacute T waves
The earliest signs of acute myocardial infarction are subtle
and include increased T wave amplitude over the affected area.
T waves become more prominent, symmetrical, and pointed
(“hyperacute”). Hyperacute T waves are most evident in the
anterior chest leads and are more readily visible when an old
electrocardiogram is available for comparison. These changes
in T waves are usually present for only five to 30 minutes after
the onset of the infarction and are followed by ST segment
changes.


ST segment changes
In practice, ST segment elevation is often the earliest recognised
sign of acute myocardial infarction and is usually evident within
hours of the onset of symptoms. Initially the ST segment may
straighten, with loss of the ST­T wave angle . Then the T wave
becomes broad and the ST segment elevates, losing its normal
concavity. As further elevation occurs, the ST segment tends to
become convex upwards. The degree of ST segment elevation
varies between subtle changes of < 1 mm to gross elevation of > 10 mm.



Pathological Q waves
As the acute myocardial infarction evolves, changes to the QRS
complex include loss of R wave height and the development of
pathological Q waves.
Both of these changes develop as a result of the loss of
viable myocardium beneath the recording electrode, and the
Q waves are the only firm electrocardiographic evidence of
myocardial necrosis. Q waves may develop within one to two
hours of the onset of symptoms of acute myocardial infarction,
though often they take 12 hours and occasionally up to 24
hours to appear. The presence of pathological Q waves,
however, does not necessarily indicate a completed infarct. If
ST segment elevation and Q waves are evident on the
electrocardiogram and the chest pain is of recent onset, the
patient may still benefit from thrombolysis or direct
intervention.
When there is extensive myocardial infarction, Q waves act
as a permanent marker of necrosis. With more localised
infarction the scar tissue may contract during the healing
process, reducing the size of the electrically inert area and
causing the disappearance of the Q waves.



Resolution of changes in ST segment
and T waves
As the infarct evolves, the ST segment elevation diminishes and
the T waves begin to invert. The ST segment elevation
associated with an inferior myocardial infarction may take up to
two weeks to resolve. ST segment elevation associated with
anterior myocardial infarction may persist for even longer, and
if a left ventricular aneurysm develops it may persist indefinitely.
T wave inversion may also persist for many months and
occasionally remains as a permanent sign of infarction.



Reciprocal ST segment depression

ST segment depression in leads remote from the site of an
acute infarct is known as reciprocal change and is a highly
sensitive indicator of acute myocardial infarction. Reciprocal
changes are seen in up to 70% of inferior and 30% of anterior
infarctions.
Typically, the depressed ST segments tend to be horizontal
or downsloping. The presence of reciprocal change is
particularly useful when there is doubt about the clinical
significance of ST segment elevation.

Reciprocal change strongly indicates acute infarction, with a
sensitivity and positive predictive value of over 90%, though its
absence does not rule out the diagnosis.
The pathogenesis of reciprocal change is uncertain.
Reciprocal changes are most frequently seen when the infarct is
large, and they may reflect an extension of the infarct or occur
as a result of coexisting remote ischaemia. Alternatively, it may
be a benign electrical phenomenon. The positive potentials that
are recorded by electrodes facing the area of acute injury are
projected as negative deflections in leads opposite the injured
area, thus producing a “mirror image” change. Extensive
reciprocal ST segment depression in remote regions often
indicates widespread arterial disease and consequently carries
a worse prognosis.



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Thursday, November 17, 2011

ST Elevation


Knowledge

The ST level is measured relative to the PR interval. While the U-P level theoretically would be preferred it cannot be used because it disappears with tachycardia. When there is a short PR interval, it can be particularly difficult for computer algorithms to find the isoelectric reference level. The direction of the ST vector and the relative position of the electrode measuring the vector determine whether the ST amplitude is positive (elevation) or negative (depression). For instance at rest, since the main ST vector projects along the long axis of the heart toward the apex, AVR will register a negative ST amplitude and V5 will register a positive ST amplitude (early repolarization). With tachycardia or ischemia the direction changes, as does the ST amplitude. As for any vector shift that is perpendicular to an electrode, no amplitude will be registered. Pathological processes that cause ST elevation shift the entire vector from it's long axis of the heart orientation and move it through the area of inflammation (pericarditis) or transmural ischemia (infarction or spasm). Thus, pathological ST depression does not localize but reflects a global subendocardial process while pathological elevation occurs directly over the involved area.
It is important to determine if the ST elevation was documented on previous ECGs and if the ST level is currently changing or is stable.
  • Acute or dynamic ST elevation can be due to severe transmural ischemia secondary to thrombus, spasm or a tight fixed coronary artery lesion or a combination of these situations. It can be the first ECG manifestation of an evolving myocardial infarction and it represents the ECG criteria for thrombolytic therapy. However, if the pain does not persist, it more likely is due to variant or unstable angina. The elevation localizes the ischemic lesion to the coronary artery supplying the area of myocardium reflected by the ECG leads. It represents transmural ischemia and is very arrythmogenic.
  • Chronic or persistent ST elevation could be due to an aneurysm when it occurs over Q waves or to chronic pericarditis (i.e., with uremia), but it most commonly occurs with a normal ECG pattern and is known as early repolarization. It may actually be due to late depolarization and is a very normal finding even to 3-4 mm in amplitude. Normally early repolarization lessens with increases in heart rate while ischemic ST elevation increases.

Recommendations

If the ST elevation has been present on prior ECGs:
If the ST elevation has been present on prior ECGs, the ECG does not exhibit diagnostic Q waves (no Q wave is wider than 35 millisec or 25% larger than the following R wave), and the elevation lessens with increases in heart rate then the benign finding of early repolarization is probable. The ECG with this finding usually will be obtained in a healthy, asymptomatic individual but it can also be obtained in a patient presenting with non-cardiac chest pain or with complaints due to another pathological process which makes the diagnosis more complicated. In this later circumstance, the early repolarization does not rule out a cardiac process but makes other diagnoses more likely.
If the ST elevation has been present on prior ECGs and occurs over diagnostic Q waves (Q wave wider than 35 millisec and 25% larger than the following R wave), a LV aneurysm or large wall motion abnormality is likely. In the case of an anterior location (i.e., V1-4), an abnormal precordial movement may be noted on examination. An echocardiogram would be the best way to evaluate LV function to see if an ACE inhibitor or other vasodilator was necessary to improve survival and lessen admissions for CHF.
When the ST elevation is a new finding:
The patient must be carefully questioned regarding ischemic symptoms including angina pectoris, chest pain, and shortness of breath, chest squeezing or pressure.
q      If the symptoms are consistent with myocardial ischemia, an aspirin and nitrates should be given immediately. If due to coronary spasm, the symptoms and elevation should resolve. If they do not, then thrombolysis should be given unless there are contraindications (bleeding disorder, recent stroke, operation or bleeding, etc). Enzymes should be drawn but treatment need not be delayed for their analysis. The ECG often also exhibits increased R and T wave amplitudes and the elevation usually is in the area of the coronary artery with spasm or thrombus.
q      If the patient's pain is pleuritic and positional, then consider pericarditis. A history of a URI or pneumonia, prior pericarditis, auto-immune disease and arthritis support the diagnosis of pericarditis. Physical exam may reveal a multi-component rub. ECG findings that also support pericarditis are PR depression, low amplitude T waves and ST elevation in multiple areas. If diagnosed, laboratory studies are indicated including renal function for uremia and patients should be closely followed for cardiac tamponade (distant heart sounds, narrow pulse pressure, pulsus paradoxus, hypotension). Echocardiography and cardiology consultation is usually indicated.
q      If the patient is asymptomatic, then the most likely diagnosis is Early Repolarization. To confirm this, the ECG can be repeated to see if the pattern is stable. "Silent Ischemia" , ischemia occurring without symptoms, is a rare possibility that usually need not be considered.

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Tuesday, November 15, 2011

Denis’ three column concept of spine stability




Stable spine is one which after the initial injury does not get displaced further. The spine is stable when atleast 2 columns of the spine are intact.

Denis’ three column concept of spine stability
According to the three column concept, the spine is considered to have 3 columns:

Anterior
Middle
Posterior


The anterior column is composed of:
Anterior longitudinal ligament
Anterior half of vertebral body and intervertebral disc


The middle column is composed of:
Posterior longitudinal ligament
Posterior half of vertebral body and intervertebral disc


The posterior column is composed of:
Transverse process
Spinous process
Pedicle
Lamina
Faceted joints
Interspinous ligament
Supraspinous ligament
Ligamentum flavum


Spinal injury and Three column concept:
One column injury is stable
Two column injury is unstable
Three column injury is invariably unstable



In adition to proposing the 'three column spine' Denis also defined four types of spinal fractures;
  • wedge fracture - stable
  • burst fracture - stable
  • seat belt fracture (and 'Chance fracture') - unstable
  • fracture dislocation - unstable

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Standard Neurological Classification of Spinal Cord Injury

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Saturday, November 12, 2011

Summary of Antibiotics‏

Tq Dr Edel (EDHUSM Resident) for this nice summary :)

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Monday, November 7, 2011

Trauma Resus: Part I

Source: http://emcrit.org/podcasts/trauma-resus-part-i/
Thought we’d talk about some trauma stuff, specifically the resuscitation of the critically ill hemorrhagic shock patient.
There is much to discuss, so this will be a multi-episode affair.
Today, we’ll concentrate on the Lethal Triad and BP Goals.

Lethal Triad

lethal EMCrit Podcast 12   Trauma Resus: Part I
The picture says it all.
Bleeding causes acidosis, hypothermia, and coagulopathy. Then the cycle begins as they all beget each other. If this continues for too long, it is irreversible.
We can iatrogenically make things worse by keeping our patients exposed and infusing ice cold fluids and products. By diluting their existing clotting factors and platelets with too much fluid and red cells. And by not ensuring adeqaute perfusion to counter acidosis.

BP Goals

Your goal is a MAP of 65. This is not hypotensive resus, which is still not proven. It is normotensive resuscitation; beyond 65, no additional benefts will be seen, but you do risk increased bleeding and dilutional coagulopathy.
If MAP < 65 – give fluids/products
If MAP > 65 – check perfusion
there are monitors for this such as NIRS measurement of thenar eminence, but at this stage, I recommend using the presence of a nice strong pulse and warm hands.
MAP > 65 & Good Perfusion-stand tight
MAP > 65 & Bad Perfusion-give fentanyl 20-25 mcg
why fentanyl? b/c taking away pain and fear will limit endogenous catecholamines and the pt’s bp will drop slightly from vasodilation. Now give fluids/products to take the MAP to > 65.
Here are the articles
resus of crit ill trauma patients
damage_control_anesthesia

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Sunday, November 6, 2011

Psychogenic Coma

Source:http://emphysicaldiagnosis.com/2011/08/09/psychogenic-coma-and-malingering/ I have now heard several stories of prisoners faking a coma. In one, he was intubated for a GCS of 8, and the first clue was that the television was mysteriously and seemingly autonomously rotated toward the patient. Eventually they lay a trap involving blocking access to the television, and were able to catch him in the act. Patients do of course lie to us, but many patients have psychogenic coma, where they are not intentionally fabricating the coma, which arises from psychological distress and is termed a conversion reaction. How can physical diagnosis demonstrate to us that a patient is actually awake? Apparently the oculocephalic (doll’s eye) responses can give either fixed eyes or reflex responses. However, the cold caloric oculovestibular reflexes are thought to be highly sensitive and specific, though they appear not to have been studied in this population. Irrigate an ear with 60-100mL of ice water. A patient in a true coma with an intact brainstem shows a slow tonic deviation of the eye toward the ice. Patients with damage to the brainstem show no response. A patient who is awake shows fast phase nystagmus away from the cold ear. Plum and Posner write “it is the presence of normal nystagmus in response to caloric testing that firmly indicates that the patient is physiologically awake and that the unresponsive state cannot be caused by structural or metabolic disease of the nervous system.” Later on they do qualify this statement by suggesting that intense visual fixation might overcome this nystagmus in some situations. Other findings that are not consistent with organic disease include resistance to eye opening and rapid/active eye closure once released. Coma findings that cannot be fabricated include the slow smooth closure of opened eyelids and roving eye movements. Apparently the rolling upward of the eyeballs upon lid opening is a voluntary act, though I have not been able to find a citation for that. Dropping the arm on the face is commonly used, and usually helpful, though I have seen it give a misleading result. With a thorough history and examination, the hope is that the diagnosis will become more clear. Take home points: Fast nystagmus away from the ice indicates an awake patient Resistance to eye opening and active eye closure suggests an awake patient References: Plum and Posner The Diagnosis of Stupor and Coma. This is a classic text that is highly recommended.

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Friday, November 4, 2011

ED extubation protocol

Source:http://emcrit.org/podcasts/extubation/

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Thursday, November 3, 2011

When to wean the CPAP in SCAPE

Source: http://emcrit.org/blogpost/when-to-wean-cpap-scape/
SCAPE= Sympathetic Crashing Acute Pulmonary Edema


Gabe writes:
REMCS notification of an obese female in her 50s being brought in on CPAP for resp distress, history of CHF, tachypneic and tachycardic.
Immediate page for respiratory to bring down NIV.
When she came through the ambulance bay, I categorized her immediately (thanks to your podacst): SCAPE. Tachycardic, hypertensive, tachypneic, diaphoretic, and severely agitated saturating upper 80s with crackles to her apices. With intubation gear ready, I placed her on a PEEP of 8 and dropped at SL NTG 0.4mg under her tongue (couldn’t get the IV nitro in time) and gave 50mcg fentanyl.
2 minutes later: RR 24 (from 40s), sat 100%, HR 80s, dry skin, and talking to us behind the CPAP. My attending was so proud and, quite frankly, relieved at not having to intubate an impossible airway.
My question is: once the patient has stabilized on the NIV, do we wean it down? Switch to NRB? Leave it to the CCU?
Thanks!
Gabe, Great question!
Here is how I wean the CPAP on these folks:
  • The patient must look good–I mean really good before I’ll even think of turning the dial. No diaphoresis, no labored breathing, can talk to you easily under the mask.
  • The blood pressure must have dropped to the patient’s norm or what you think is the patient’s norm.
  • The nitro drip must have done its precipitous drop thing, by which I mean, at some point these SCAPE patients turn off their sympathetic surge. Their nitro drip necessity will go from a level such as 180 mcg/min to 30 mcg/min. Once that happens, you know you are over the hump.
  • When all of the above have occurred, I drop the fiO2 to 40% and then I start weaning down the PEEP setting about 2 cmH20 every 5-10 minutes.
  • Check the patient for the above before each subsequent PEEP drop.
  • When they are at 5 cmH20, give them a trial of nasal cannula.
  • Keep the entire CPAP set-up ready at the bedside
  • If the patient’s BP spikes or they get sweaty and are having trouble breathing, put them back on CPAP and go back up on your nitro.
  • Now is the time to assess whether you think they are volume overloaded and if you think it is clever, give them a diuretic. For me I’d rather they get their kidneys going with the nitro instead of the diuretic.

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Was established since 25 Nov 09.Just to educate myself.

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