Friday, December 2, 2011
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).
Sunday, November 20, 2011
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.
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.
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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
Saturday, November 12, 2011
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
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 Read more...
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.
Read more...Friday, November 4, 2011
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.
Read more...
Tuesday, October 25, 2011
Ventilator settings for acute lung injury and ARDS
Source:http://academiclifeinem.blogspot.com/2011/10/paucis-verbis-ventilator-settings-for.html
Ventilator settings for obstructive lung disease
Source:http://academiclifeinem.blogspot.com/2011/10/paucis-verbis-ventilator-settings-for_21.html
Sunday, September 11, 2011
Distracting injuries in c-spine injuries
Saturday, August 27, 2011
Subclavian Vein Catheterization Techniques
The technique is identical to that described above for internal jugular vein cannulation except for the puncture site. Two techniques, infraclavicular and supraclavicular, are described below and summarized in Table 38-7.
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Infraclavicular Approach to the Subclavian Vein
The infraclavicular approach to the subclavian vein is most often used. It is commonly thought to be easier to perform and less likely to result in a pneumothorax than the supraclavicular approach, although data for this belief are lacking.17 Some physicians prefer not to use a finder needle for infraclavicular subclavian vein cannulation as there is no danger of penetrating the carotid artery. This also makes as few needle passes near the pleura as possible in order to decrease the risk of a pneumothorax. Estimate the distance from the skin puncture site to the superior vena cava (i.e., the manubriosternal junction).
Several different skin entry sites are described in the literature. Some feel that the preferred entry site is 1 cm caudal to the junction of the medial and middle thirds of the clavicle. The subclavian vein lies just posterior to the clavicle at this site. The first rib lies between the pleural dome and the subclavian vein. Direct the introducer needle just superior and posterior to the suprasternal notch while staying as close to the frontal (coronal) plane as possible. The needle and syringe should be parallel to the bed (Figure 38-14). Placing the nondominant index finger in the sternal notch will help to guide placement (Figure 38-14).
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Some practitioners prefer to enter the skin inferior to the clavicle at the deltopectoral groove, or the point just lateral to the midclavicular line along the inferior surface of the clavicle. This is the point where the skin may be maximally depressed. Direct the introducer needle parallel to the bed and toward the sternal notch. This entry site may make it easier to keep the introducer needle in the coronal plane. The distance before entering the subclavian vein is longer than in the preceding approach and the protection offered by the first rib is lost.
One of the editors (R.R.S.) prefers to use a different landmark. Palpate the bony tubercle, or protrusion, on the inferior surface of the clavicle and approximately one-third to one-half the length of the clavicle from the sternoclavicular joint. The advantage of this site is that it is a definitive landmark and avoids approximating distances, as described for the other sites above. Insert the introducer needle parallel to the bed and aimed just posterior to the sternal notch.
The bevel of the introducer needle should be oriented caudally, as should the "J" in the guidewire. This position will allow the guidewire to enter the innominate vein and superior vena cava rather than being directed upward into the internal jugular vein or across to the contralateral subclavian vein (Figure 38-15). Once venous blood is aspirated, the Seldinger technique for catheter insertion is otherwise the same as previously described for internal jugular vein cannulation. Aspiration of bright red blood under pressure indicates subclavian artery puncture, which will be incompressible. Remove the introducer needle and observe the patient for signs of significant hemorrhage over the next several hours. Aspiration of air indicates penetration of the pleura. Observation with serial chest radiographs for at least the next 6 to 24 hours is essential to evaluate the size of the resulting pneumothorax.
Read more...Thursday, August 25, 2011
Hypertension-Malaysian CPG
Hypertension is defined as persistent elevation of systolic BP of
140 mmHg or greater and/or diastolic BP of 90 mmHg or greater.
The classification is based on the average of two or more readings
taken at two or more visits to the doctor. When SBP and DBP fall
into different categories, the higher category should be selected to
classify the individual’s BP.
Definition of prehypertension
Prehypertension is defined as systolic BP (SBP) 120 to 139 or
diastolic BP (DBP) 80 to 89 mmHg, based on 2 or more properly
measured seated BP readings on each of 2 or more office visits.
If BP is still >140/90 mmHg with three drugs, including a
diuretic at near maximal doses, patients by definition have
resistant hypertension.
Efforts must be made to reach target BP. For patients <65 years old, the
target BP should be <140/85 mmHg and <130/80 mmHg for
diabetics.In general once the BP is controlled, most patients will require life-long
treatment.
SEVERE HYPERTENSION
Definition:
Severe hypertension is defined as BP >180/110 mmHg.
These patients may present in the following manner:
• incidental finding in an asymptomatic patient
• non-specific symptoms like headache, dizziness, lethargy
• symptoms and signs of acute target organ damage. These
include acute heart failure, acute coronary syndromes, acute
renal failure, dissecting aneurysm, hypertensive encephalopathy
and stroke
Patients are then categorised as having:
a) asymptomatic severe hypertension,
b) hypertensive urgencies, or
c) hypertensive emergencies
(b) and (c) are also referred to as hypertensive crises.
Asymptomatic severe hypertension:
Admission may be necessary in the newly diagnosed, or where
compliance may be a problem. Patients already on treatment need
to have their drug regime reviewed.
Hypertensive urgencies:
-These include patients with grade III or IV retinal changes (also
known as accelerated and malignant hypertension respectively), but
no overt organ failure. These patients may need admission.
-BP measurement should be repeated after 30 minutes of bed rest.
- Grade 1
- Generalised arteriolar constriction - seen as `silver wiring` and Vascular tortuosities.
- Grade 2
- As grade 1 + irregularly located, tight constrictions - Known as `AV nicking` or `AV Nipping`
- Grade 3
- As grade 2 + with cotton wool spots and flame-haemorrhages
- Grade 4
- As above but with swelling of the optic disk (papillodema)
There is an association between the grade of retinopathy and mortality. At 3 years 70% of those with grade 1 retinopathy will be alive whereas only 6% of those with grade 4 will survive.[1]Grading of the retinopathy is thus important as the hypertensive process will be affecting small vessels throughout the body in a similar manner. (The retina is simply the most visible area to assess.)
-Initial treatment should aim for about 25% reduction in BP over 24 hours
but not lower than 160/90 mmHg. (Level III)
- Oral drugs proven to be
effective are outlined in Table 10. Combination therapy is often
necessary.
Hypertensive emergencies:
-These include patients with complications of severe hy
pertension
such as acute heart failure, dissecting aneurysm, acute coronary
syndromes, hypertensive encephalopathy, subarachnoid
haemorrhage and acute renal failure.
-These may occur in patients with BP <180/110 mmHg, particularly if the BP has risen rapidly.
-All these patients should be admitted.
-The BP needs to be reduced rapidly. It is suggested that the BP
be reduced by 25% depending on clinical scenario over 3 to 12 hours but not lower than 160/90 mmHg
-This is best achieved with parenteral drugs.
Dangers of rapid reduction in blood pressure:
Rapid reduction of BP (within minutes to hours) in asymptomatic
severe hypertension or hypertensive urgencies is best avoided as
it may precipitate ischaemic events.
Monday, August 22, 2011
Sore Throat: Modified Centor Score and Clinical Decision Rule
Source:http://emergencywebnotes.blogspot.com/2011/08/group-beta-haemolytic-streptococcus.html
Subungual Hematoma Drainage
1.Prepare the finger with Betadine
2.Using the preferred tool for nail penetration, make a hole at the base of the nail or in the center of the hematoma. This hole must be large enough for the hematoma to drain.
3.If using an 18-ga needle, twirl the needle between the thumb and index finger with slight downward pressure until no resistance is felt and dark blood return is seen from the hole.
4.If using a paper clip, first heat the end of the paper clip in open flame to sterilize it. Apply the hot tip to the nail until resistance is no longer felt and blood return is seen.
If using a sterile cautery tool, activate cautery until the tip is hot. Apply the tool to the nail as with a heated paper clip.
5.Allow the hematoma to drain. Gentle squeezing at the tip of the finger may facilitate hematoma drainage.
6.Apply antibacterial ointment (eg, bacitracin) over the trephination site and dress the wound with gauze or an adhesive bandage.
Pearls
1.When appropriate, take a radiograph of the finger to rule out an underlying fracture that may require splinting.
2.Always check for the presence of an associated extensor tendon injury.
3.Hematomas that are larger than 50% of the nail do not necessarily require nail removal and exploration.
4.The nail may fall off during the week following hematoma drainage but should regrow as long as the germinal matrix is intact.
5.Multiple holes may be necessary to facilitate adequate drainage.
Drainage of the subungual hematoma does not accelerate healing or prevent infection.
If the heat of an electrocautery device is painful for the patient (which is not typical), an 18-ga needle should instead be used for trephination.
Source:http://emedicine.medscape.com/article/82926-overview#a15
Sunday, August 21, 2011
BLEED Criteria for UGIB and LGIB
Conclusion:
The BLEED classification, applied at initial emergency department evaluation and before admission, predicts hospital outcomes for patients with acute upper or lower GI hemorrhage. This outcome prediction tool also identified variations in intensive care utilization between two hospitals.
Source:http://www.ncbi.nlm.nih.gov/pubmed/9233736
Saturday, August 20, 2011
An approach to persistent tachycardia
Source:http://academiclifeinem.blogspot.com/2011/08/paucis-verbis-approach-to-persistent.html
Monday, August 15, 2011
PE-McConnell`s sign
Source:http://lifeinthefastlane.com/2010/09/cardiovascular-curveball-011/
A 35 year-old female is brought to the emergency department after collapsing in a shopping centre. Paramedics found her to be GCS 3 and shortly afterwards required CPR and 1mg adrenaline for profound bradycardia and no pulse. Spontaneous output returned and no further drugs have been required to support her circulation. She remains intubated and GCS 3. There is little other history, except some information from a friend stating she had been on a trip to South America recently.
Read more...
You perform a quick bedside echo while the paramedics are changing over their monitoring.
Questions
Q1. What are the obvious abnormalities on this echo?
- Small LV cavity size with normal LV systolic function
- Septal flattening consistent with RV pressure overload
- Severely dilated RV with severely reduced systolic function
Q2. What is McConnell’s sign?
- Echocardiographic pattern of RV dysfunction consisting of akinesia of the mid free wall but normal motion at the apex
- 77% sensitivity and 94% specificity for diagnosis of pulmonary embolism
Q3. What are the echocardiographic features of right ventricular dysfunction in acute pulmonary embolism?
- RV wall hypokinesis
- Moderate or severe
- McConnell’s sign
- RV dilatation
- End-diastolic diameter >30 mm in parastemal view
- RV larger than LV in sobcostal or apical view
- Increased tricuspid velocity >26 m/sec
- Paradoxical RV septal systolic motion
- Pulmonary artery hypertension
- Pulmonary artery systolic pressure >30 mmHg
- Dilated IVC with lack of respiratory collapse
Other echocardiographic features associated with increased mortality include patent foramen ovale and free-floating right-heart thrombus.
Q4. What are the indications for thrombolysis in acute pulmonary embolism?
Fibrinolysis in acute pulmonary embolism remains a controversial topic.
- Most agree that cardiac arrest and haemodynamic instability (SBP < 90mmHg) are indications for thrombolysis.
- Controversy surrounds thrombolysis for stable patients with RV dysfunction on echocardiography.
- Treatment in this group has been shown to decrease pulmonary artery pressure and improve RV systolic function and pulmonary perfusion
- This benefit must be weighed against the risk of haemorrhage with thrombolytic therapy.
- Thrombolysis has not been shown to improve mortality.
- Other treatment algorithms include the use of elevated Troponin and BNP to select which patients require urgent echocardiography
In haemodynamically stable patients with RV dysfunction, thrombolysis should be considered on a case-by-case basis
Q5. What would you do next?
- Administer thrombolysis
- Although stable at the moment, this patient has had a cardiac arrest from a pulmonary embolus and is potentially very unstable
- She has severe RV dysfunction on echocardiography
- There are no obvious contraindications to thrombolysis
- Alteplase 50mg IV bolus
Q6. What was the response to treatment?
- This echo was performed a few hours later. Already some improvement in RV dysfunction is evident.
This case illustrates the utility of bedside echocardiography in the emergency department. Using the clinical history, a diagnosis of massive pulmonary embolism was made at the bedside and appropriate treatment could be administered almost immediately.
The pictures are from a real case, with some of the details changed. Let’s just say that thrombolysis makes failed intubation interesting ……..
Wednesday, August 10, 2011
Corneal Abrasion vs Corneal ulcer
A corneal abrasion is an injury to the epithelium that is superficial enough not to involve the basement membrane. It is due to mechanical trauma. The defect is seen as superficial on slit lamp and takes up fluorescein, shining green upon illumination with cobalt blue light.
Note that corneal abrasions generally do not cause scarring upon healing because the Bowman’s membrane is not violated.
Corneal ulcer is a defect that involve the stroma, past Bowman’s membrane. It is usually infected (with few exceptions, like the sterile ulcers seen in Vernal Catarrh due to releases of toxic inflammatory mediators), and leaves a scar upon healing. It shows as a more or less deep corneal defect with infiltrates in the ulcer bed as well as around it, with sometimes pus and tissue melting. It surely takes up fluorescein. Cultures should be taken from the ulcer prior to initiating treatment, which include specially prepared fortified doses of antibiotics eye drops, like Tobramicin and Kefzole together, or Amikacin and Vancomycin, to be used as frequently as Q1/2 hr to 1 hr, awaiting for the cultures to be out. Microorganisms recovered are Staph and Strep, Pseudomonas (especially in contact lens wearers and ICU patients), fungi (amphotericin eye drops hance to be used), or acanthameoba. An ulcer is NEVER patched, unlike an abrasion. If an ulcer is axial, the final outcome after healing could be poor vision because of scarring, necessitating corneal transplant (Penetrating Keratoplasty ). The use of topical steroids in conjunction to antibiotics once the ulcer approaches healing is beneficial to decrease scarring from the inflammatory reaction elicited and hence reach better visual outcome.
Treatment is usually prophylactic antibiotics with pressure patching over 24 hours to decrease the mechanical movement of the blinking lid and moving globe, which disrupt the epithelial network trying to heal the defect. Antibiotics are usually broad spectrum eye drops or ointments, like erythromicin, fucithalmic, polymixin/sulfacetamide. If the foreign object causing the abrasion is wood, twig, and so on, the use of polymixin/trimethoprim is more judicious to cover fungi as well.
CT/MRI criteria for acute/chronic hydrocephalus
CT/MRI criteria for acute hydrocephalus include the following:CT/MRI criteria for chronic hydrocephalus include the following:
Marshall CT classification of TBI
Source:http://bja.oxfordjournals.org/content/99/1/18/T7.expansion.html
Marshall Classification of Diffuse Brain Injury
Grade 1 = normal CT scan (9.6% mortality)
Grade 2 = cisterns present, shift < 5mm (13.5% mortality)
Grade 3 = Cistern compressed/ absent, shift <5mm (34% mortality)
Grade 4 = Shift > 5mm (56.2% mortality)
Marshall LF, Bowers-Marshall S, Klauber MR et al. A new classification of head injury based on computerized tomography. J Nuerosurg 75(Suppl):S14-20, 1991
Saturday, July 30, 2011
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