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.

Table 38-7. Comparison of Subclavian Vein Cannulation Routes

Infraclavicular approach Supraclavicular approach Entry site Just inferior to the clavicle at the midclavicular line 1 cm lateral to the clavicular head of the sternocleidomastoid muscle, 1 cm posterior to the clavicle Needle orientation Keep as close to the coronal plane as possible Tip aimed 10 degrees anterior to the coronal plane Needle bevel and "J" wire directed (FIG) Medially and caudally Medially Aim toward Just posterior to the sternal notch Contralateral nipple, needle bisects angle formed by the clavicle and the clavicular head of the sternocleidomastoid muscle Distance from skin to subclavian vein 3–4 cm 2–3 cm

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).

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.

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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.

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Sore Throat: Modified Centor Score and Clinical Decision Rule

Source:http://emergencywebnotes.blogspot.com/2011/08/group-beta-haemolytic-streptococcus.html

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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

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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

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An approach to persistent tachycardia

Source:http://academiclifeinem.blogspot.com/2011/08/paucis-verbis-approach-to-persistent.html

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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.

You perform a quick bedside echo while the paramedics are changing over their monitoring.

Questions

Q1. What are the obvious abnormalities on this echo?

Answer and interpretation

• 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?

Answer and interpretation

• 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?

Answer and interpretation

• 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?

Answer and interpretation

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?

Answer and interpretation

• 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?

Answer and interpretation

• 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 ……..

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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.
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.

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.

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CT/MRI criteria for acute/chronic hydrocephalus

• CT/MRI criteria for acute hydrocephalus include the following:

  • Size of both temporal horns is greater than 2 mm, clearly visible. In the absence of hydrocephalus, the temporal horns should be barely visible.
  • Ratio of the largest width of the frontal horns to maximal biparietal diameter (ie, Evans ratio) is greater than 30% in hydrocephalus.
  • Transependymal exudate is translated on images as periventricular hypoattenuation (CT) or hyperintensity (MRI T2-weighted and fluid-attenuated inversion recovery [FLAIR] sequences).
  • Ballooning of frontal horns of lateral ventricles and third ventricle (ie, "Mickey mouse" ventricles) may indicate aqueductal obstruction.
  • Upward bowing of the corpus callosum on sagittal MRI suggests acute hydrocephalus.
• CT/MRI criteria for chronic hydrocephalus include the following:

  • Temporal horns may be less prominent than in acute hydrocephalus.
  • Third ventricle may herniate into the sella turcica.
  • Sella turcica may be eroded.
  • Macrocrania (ie, occipitofrontal circumference >98^th percentile) may be present.
  • Corpus callosum may be atrophied (best appreciated on sagittal MRI). In this case, parenchymal atrophy and ex-vacuo (rather than true) hydrocephalus from a neurodegenerative disease should be considered.

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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

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