Did I Ask For It Stat?

DCR

2011-05-04T20:01:00.000-07:00

DCR = cardioversion (direct current reversion)

References

Pantoprazole infusion

2011-05-04T04:53:00.000-07:00

For actively bleeding ulcers give pantoprazole bolus followed by infusion.

LOading dose: Pantoprazole 80mg IV in 100ml of NaCl 0.9% or 5% glucose over 20 - 30 minutes
Infusion:

Pantoprazole 200mg in Dextrose 5% 500mL at 20mL/hr (each mL is 0.4mg , 20mL/hr = 8mg/hr, 1mg =2.5mL)
Pantoprazole 80mg in N/Saline 100mL at 10mL/hr (each mL is 0.8mg , 10mL/hr = 8mg/hr,1mg=1.25mL)

References

Pantoprazole infusion guidelines, http://www.philippelefevre.com/JHH-ICU-guidelines/adult-drug-infussions/pantoprazole-infusion.pdf
Pantoprazole Infusion as Adjuvant Therapy to Endoscopic Treatment in Patients With Peptic Ulcer Bleeding: Prospective Randomized Controlled Trial, medscape.com

Blood Gas normal values

2011-01-25T00:22:00.000-08:00

	Arterial	Venous
pH	7.35-7.45	7.3-7.35
pCO2	35-45	45-46 (good representation of ventilation)
pO2	80-100	20-80 (uninterprable)
SaO2	95-100
HCO3-	22-28
BE	+/- 3

Resources for lumbar puncture

2010-12-07T03:23:00.000-08:00

http://www.med.uottawa.ca/procedures/lp/index.htm
http://www.articlealley.com/article_596234_17.html
http://www.unboundmedicine.com/harrisons/ub/view/Harrisons-Manual-of-Medicine/148408/all/Lumbar_Puncture,

Resources for central line insertion

2010-11-30T02:17:00.000-08:00

Central lines in general

http://egret.psychol.cam.ac.uk/medicine/Central_line_insertion.pdf
http://www.nda.ox.ac.uk/wfsa/html/u12/u1213_01.htm
http://www.proceduresconsult.com/medical-procedures/central-venous-line-placement-AN-procedure.aspx

Internal jugular lines

http://www.anwresidency.com/simulation/guide/ij.html

AMIs and thrombolysis

2010-05-09T18:30:00.000-07:00

ECG changes indicating AMI

High probability of MI: persistent ST elevation of ≥ 1 mm in two contiguous limb leads or ST-segment elevation of ≥ 2 mm in two contiguous chest leads or the presence of new LBBB.
Intermediate probability of MI: are ST depression, T-wave inversion, and other nonspecific ST-T wave abnormalities.
Q waves = old MI

DDxes

Aortic dissection
Pericarditis (would show on all leads)
Pulmonary embolism

Management options

Patients with persistent ST elevation should be considered for reperfusion therapy (thrombolysis or primary PCI).
Those without ST elevation will be diagnosed with either NSTEMI if cardiac marker levels are elevated or with unstable angina if serum cardiac marker levels provide no evidence of myocardial injury. Patients presenting with no ST-segment elevation are not candidates for immediate thrombolytics but should receive anti-ischemic therapy and may be candidates for PCI urgently or during admission.

Medical Management

Aspirin (300 mg) should be given unless already taken or contraindicated (grade A recommendation), and should preferably be given early (eg, by emergency or ambulance personnel).
Clopidogrel should be given in addition to aspirin for patients undergoing PCI with a stent (loading-dose of 300–600 mg), or for fibrinolytic therapy (300 mg). Clopidogrel 75 mg daily should be continued for at least a month after fibrinolytic therapy, and for up to 12 months after stent implantation, depending on the type of stent.
Antithrombin therapy to inhibit the coagulation cascade, and for patients underdoing PCI. For patients getting streptokinase, whether to heparinise depends on the anti-thrombotic agent. Clexane (enoxaparin) bolus should be dosed at 0.75 mg/kg.
Administer a platelet glycoprotein (GP) IIb/IIIa-receptor antagonist (eptifibatide, tirofiban, or abciximab) in addition to aspirin and unfractionated heparin, to patients with continuing ischemia or with other high-risk features and to patients in whom PCI is planned.
An ACE inhibitor (Captopril) should be given orally within the first 24 hours of STEMI to patients with anterior infarction, pulmonary congestion, or left ventricular ejection fraction (LVEF) less than 40% in the absence of hypotension.
An angiotensin receptor blocker (valsartan or candesartan) should be administered to patients with STEMI who are intolerant of ACE inhibitors and who have either clinical or radiological signs of heart failure or LVEF less than 40%.

Contraindications for fibrinolytic use in STEMI

Absolute contraindications:

Prior intracranial hemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed-head trauma or facial trauma within 3 months

Relative contraindications:

History of chronic, severe, poorly controlled hypertension
Severe uncontrolled hypertension on presentation (SBP >180 mm Hg or DBP >110 mm Hg)
Traumatic or prolonged (>10 min) CPR or major surgery less than 3 weeks
Recent (within 2-4 wk) internal bleeding
Noncompressible vascular punctures
For streptokinase/anistreplase - prior exposure or prior allergic reaction to these agents
Pregnancy
Active peptic ulcer
Current use of anticoagulant (eg, warfarin sodium) that has produced an elevated international normalized ratio (INR) >1.7 or prothrombin time (PT) >15 seconds

Follow-up Patient Care

Patients should continue to receive beta-blockers, nitrates, and heparin, as indicated.
ACE inhibitors have been shown to improve survival rates in patients who have experienced an MI. In the acute setting, afterload reduction from ACE inhibitors may reduce the risk of CHF and sudden death.

References

Guardianship

2010-03-12T16:23:00.000-08:00

If a patient refuses treatment...

If NOK agrees not to treat → OK but document it
If NOK thinks treatment should occur → need to go to guardianship tribunal

Antibodies

2010-01-17T14:10:00.000-08:00

Antibodies consist of two Ig heavy chains (blue) linked by disulfide bonds to two Ig light chains (green).

Heavy chains

Heavy chains define the class of immunoglobulin. There are 5 types of heavy chains:

α (Ig A)
δ (Ig D)
ε (Ig E)
γ (Ig G)
μ (Ig M)

The immunoglobulin heavy chain gene complex has been assigned to chromosome 14.

Light chains

There are 2 types of light chains:

Lambda (λ) - encoded by a gene on chromosome 22
Kappa (κ) - encoded by a gene on chromosome 2

Ig light chains produced in neoplastic plasma cells (e.g. in multiple myeloma) are called Bence Jones proteins.

References

http://en.wikipedia.org/wiki/Immunoglobulin_heavy_chain
http://en.wikipedia.org/wiki/Immunoglobulin_light_chain
http://en.wikipedia.org/wiki/Multiple_myeloma#Pathophysiology
http://www3.interscience.wiley.com/journal/120047597/abstract?CRETRY=1&SRETRY=0

Well’s Criteria for DVT

2010-01-15T23:06:00.000-08:00

The Score

Active cancer (treatment within last 6 months or palliative) -- 1 point
Calf swelling >3 cm compared to other calf (measured 10 cm below tibial tuberosity) -- 1 point
Collateral superficial veins (non-varicose) -- 1 point
Pitting edema (confined to symptomatic leg) -- 1 point
Swelling of entire leg - 1 point
Localized pain along distribution of deep venous system—1 point
Paralysis, paresis, or recent cast immobilization of lower extremities—1 point
Recently bedridden > 3 days, or major surgery requiring regional or general anesthetic in past 4 weeks—1 point
Alternative diagnosis at least as likely—Subtract 2 points

Possible score -2 to 8

Interpretation

Score of 2 or higher - deep vein thrombosis is likely. Consider imaging the leg veins.
Score of less than 2 - deep vein thrombosis is unlikely. Consider blood test such as d-dimer test to further rule out deep vein thrombosis.

References

http://en.wikipedia.org/wiki/Deep_vein_thrombosis
http://emedicine.medscape.com/article/758140-overview

CHAD2 (CHADS) score

2010-01-12T21:47:00.000-08:00

The CHADS score is a clinical prediction rule for estimating the risk of stroke in patients with non-rheumatic atrial fibrillation (AF) and is used to determine the degree of anticoagulation therapy required.

To Score...

C ongestive heart failure (1 point)
H ypertension > 160mmHg systolic (or treated hypertension) (1 point)
A ge > 75 (1 point)
D iabetes (1 point)
S - previous stroke or TIA (2 points)

Risk of stroke based on CHADS score

Recommendations for anticoagulation

High risk (score >= 2) - warfarin (unless contrainidcated)
Moderate risk (score 1) - aspirin or warfarin
Low risk (score 0) - aspirin

References

http://en.wikipedia.org/wiki/CHADS_Score
http://www.cardiology.org/tools/risk_of_stroke_AF.html

ABCD^2 (ABCD squared) post TIA stroke risk assessment tool

2010-01-08T17:04:00.000-08:00

The Tool

AGE: greater than or equal to 60 years – 1 point
Blood Pressure: Systolic >= 140, diastolic >= 90 (when first assessed after TIA) – 1 point
Clinical Features: unilateral weakness – 2 points, isolated speech disturbance – 1 point, other – zero
Duration of TIA symptoms: greater than or equal to 60 minutes – 2 points, 10 to 59 minutes – 1 point, <10 minutes zero
Diabetes present – 1 point

Estimated two day stroke risks determined by the ABCD^2 score:

Score 6 to 7: High two day stroke risk (8.1%)
Score 4 to 5: Moderate two day stroke risk (4.1%)
Score 0 to 3: Low two day stroke risk (1.0%)
Score < 1: Very low two day stroke risk (0.0%)

In versus outapatient management

People with a high risk of stroke (ABCD2 score of 4 or above) should have:

Aspirin (300 mg daily) started immediately
specialist assessment and investigation within 24 hours of onset of symptoms
measures for secondary prevention introduced as soon as the diagnosis is confirmed, including discussion of individual risk factors

People who are at lower risk of stroke (ABCD2 score of 3 or below) should have:

Aspirin (300 mg daily) started immediately
specialist assessment and investigation as soon as possible, but definitely within 1 week of onset of symptoms
measures for secondary prevention introduced as soon as the diagnosis is confirmed, including discussion of individual risk factors

Investigations

CT scan without enhancement should be done in all patients to exclude other causes of neurological deficit (e.g. hemorrhage, subdural hematoma)

The presence of an infarct on CT is highly predictive of subsequent stroke

Early CT showing hemorrhage makes carotid imaging unnecessary

Carotid imaging should be done for all patients with symptoms in anterior circulation territory.

The presence of carotid disease is highly predictive of recurrent stroke.

Consider CT angiogram if Carotid Ultrasound cannot be obtained in reasonable time.

ECG and occasionally Holter monitoring to detect atrial fibrillation.
ECHO cardiogram for persons with suspect underlying cardiac abnormalities.
Blood sugar to detect extremes in glucose levels.

References

http://bmhgt.com/2009/03/stroke-information-abcd2/
http://www.gpnotebook.co.uk/simplepage.cfm?ID=x20080723164438749131
http://www.palmedpage.com/Text_files/Neurology/ABCD/TIA%20Management.html
http://www.stroke.org/site/DocServer/NSA_ABCD2_tool.pdf?docID=5981

Paediatric elbow trauma

2009-12-17T14:48:00.000-08:00

You can tell the approximate age of a child from the degree of bone replacement of cartilage on x-ray. Approximately :

Capitellum 'appears' at 2
Radial head at 4
Medial condyle at 6
Trochlea at 8
Olecranon at 10
Lateral condyle at 12 years of age

The acronym CRMTOL is used to describe the usual order of appearance of all 6 elbow centers: capitellum, radial head, medial epicondyle, trochlea, olecranon, and lateral epicondyle.

References

http://www.pediatric-orthopedics.com/Topics/Bones/Humerus/humerus.html
Elbow Trauma, Pediatric on eMedicine

Sedation tips

2009-11-18T19:05:00.000-08:00

Don't use midazolam and olanzapine together as it can cause rapid onset respiratory depression. Clonazepam and olanzipine is a better combination.
Chlorpromazine is also good. Non-addictive, and comes as a liquid.

Blood Products timing

2009-11-04T17:18:00.000-08:00

RBCs 1 unit q4h
FFP 1 unit q1h
Platelets 1 unit q30minutes

CTPA and renal function

2009-09-17T03:22:00.000-07:00

GFR < 60 is borderline.

Home Oxygen

2009-09-15T17:53:00.000-07:00

Criteria to qualify:

pO2 < 55
SaO2 < 90% RA
Non-smoker!

Can be regular/PRN.

Hartmann's (Compound Sodium Lactate)

2009-09-11T03:20:00.000-07:00

Components (in mmols):

Na 129
K 5
Ca 2
Cl 109
bicarb 29

Peutz–Jeghers syndrome

2009-08-22T21:08:00.000-07:00

Peutz–Jeghers syndrome is also known as hereditary intestinal polyposis syndrome.
An autosomal dominant genetic disease characterized by the development of benign hamartomatous polyps in the GIT and hyperpigmented macules on the lips and oral mucosa.
Prevalence of approximately 1 in 100,000 to 200,000 births.

Diagnosis

Need 2 of 3 of:

Family history
Mucocutaneous lesions causing patches of hyperpigmentation in the mouth and on the hands and feet.
- Oral pigmentations are the first to appear and play an important part in early diagnosis. Intraorally, they are most frequently seen on the gingiva, hard palate and inside of the cheek. The mucosa of the lower lip is almost invariably involved as well.
Hamartomatous polyps in the gastrointestinal tract. These are benign polyps with an extraordinarily low potential for malignancy.
Mutation in the tumour supressor gene STK11 on chromosome 19.

Natural history

Most patients will develop melanotic macules during the first year of life.
Intussusception usually first occurs between the ages of six and 18 years old.
Most people will have developed some form of neoplastic disease by age 60.

Cumulative lifetime cancer risk begins to rise in middle age.
Cumulative risks by age 70 for all cancers, gastrointestinal (GI) cancers, and pancreatic cancer are 85%, 57%, and 11%, respectively.

References

http://en.wikipedia.org/wiki/Peutz-Jeghers_syndrome
http://www.answers.com/topic/peutz-jeghers-syndrome

IV Fluids

2009-06-14T01:48:00.000-07:00

Standard fluid regime for NBM patients:

N/2 * 2 bags
4 % dextrose + N/5 + 30mmol KCl

In terms of fluid requirements,

65% of body is water (TBW)
2/3 of this is intracellular, 1/3 extracellular

Ways you can lose electrolytes:

Vomiting → loss of K
Diarrhoea→ loss of K
Sweat→ loss of NaCl
Burns → loss of protein and Na
Third space losses → loss of NaCl + H20

Ways to assess dehydration:

Urine dipstick - concentration
↑ Ur and ↑ Na

Correction of hypernatremia begins with a calculation of the fluid deficit. Predicted insensible and other ongoing losses are added to this number and the total is administered over 48 hours. Recheck serum electrolyte levels frequently during therapy. To avoid cerebral edema and associated complications, the serum sodium level should be raised by no more than 1 mEq/L every hour. In patients with chronic hypernatremia, an even more gradual rate is preferred.

Free Water Deficit (L) = Body Weight (kg) X Percentage of Total Body Water (TBW) X ([Serum Na / 140] - 1)

Percentage of TBW should be as follows:

Young men - 0.6%
Young women and elderly men - 0.5%
Elderly women - 0.4%

Example:

A serum sodium level of 155 in a 60-kg young man represents a fluid deficit of 60 X 0.6 X ([155 / 140] - 1) or 3.9 L

With another 900 mL of insensible losses, the patient requires 4.8 L of fluid in the next 48 hours, resulting in an infusion rate of 100 mL/h.

SIADH

Pure water depletion and ↑ Na → use 4% D + N/5 to treat it.
Stimulating the bowel e.g. abdo surgery → release of ADH → SIADH

References

http://www.merck.com/mmpe/print/sec12/ch156/ch156e.html
http://emedicine.medscape.com/article/766683-treatment

Psych progress notes template

2009-06-14T01:04:00.000-07:00

Day X
Meds

Subjective

What they tell you

Objective

Assessment

What do they have? Are they getting better/worse?

Plan

care level
leave

unescorted x __ hrs
escorted x __ hrs with ____

Medications - any new ones/stopped ones/changes in doses?
Investigations
Other things that need to be done e.g. call GP, family members etc..

Wounds

2008-02-27T14:07:00.001-08:00

Epidemiology of wounds

The most frequently involved body locations are the face, scalp, fingers, and hands.
~50% of traumatic lacerations seen in the ED are sustained form blunt objects.
Children have different wound epidemiologic characteristics: wounds are more likely to be located on the head which are linear, shorter, less contaminated, and more often caused by blunt trauma, compared with the wounds of adults.

Types of wounds

Contusion:

Bump or swelling arising quickly following a blow.
The surface of the skin is intact but small blood vessels are damaged →
bruising that is red at first and turns blue and finally to black.

Haematoma:
- Severe injury → blood vessels are damaged → escape of blood into tissues.
- Haematomas can be subcutaneous, in between the deeper tissues, or in the deeper tissues.
- Pressure can build up if the area is surrounded by fascial tissue → compression of blood vessels in that compartment.
- Mostly the haematomas get resolved.

Abrasion:
- Superficial layers of the skin are torn or scoured when the skin gets in contact with a
  rough surface e.g. road.
- Multiple bleeding points and sensitive nerve endings are exposed. Dust and dirt gets into the tissues.

Degloving injuries:
- Shearing forces can detach the skin from the underlying structure without damage to them.
- The skin may be lost completely or may be attached at one end to form a flap.
- In physiological degloving the skin remains intact but it is separated from the deeper structures
  e.g. when tissues are drawn into the rollers of a machine or under the tyres of a motor vehicle.
- The affected part is insensitive to painful stimulus, lacks capillary circulation and
  is pale in colour.

Incised wounds:
- Results from sharp cutting edges of knifes, glass or metal.
- The wound is near the subcutaneous fat and tissues may pout through.
- Bleeding will be profuse initially → large risk from haemorrhage.
- Contamination is relatively uncommon.

Lacerations:
- Irregular untidy wounds resulting from crushing or tearing forces.
- The laceration is surrounded by abrasion or contusion. The skin edges of the laceration are irregular may be blue or pale indicating devitalisation.
- Bleeding may not be heavy, as the blood vessels are not cleanly cut like in incised wounds.
- Underlying muscles may be damaged.
- Contamination is heavy and may result in infection.
- Foreign material may be embedded.

Puncture wounds:
- Results from stabbing action by a thin long weapon, instrument,
  object or missile/bullet where the depth of the wound is longer than the length
  of the object.
- Damage to deeper structures and organs is high and contamination leads to infection.
- A penetrating wound is when the puncture wound has no exit.
- A perforating wound is a puncture wound with an entry and exit.
Hydraulic injection injuries:
- Caused by striking of the skin & injection by liquid from hydraulic systems under very high pressure e.g. water, oil or grease.
- Large volumes may be injected.
- The entry wound is very small & sometimes difficult to identify.
Bites:
- Bites can be from animals, humans, insects or reptiles.
- Infection is one of the major risks due to mixed organisms in the mouth which gets deeply implanted into the deeper tissues.
- Tetanus is always possible in animal bites.
- Reptile and insect bites are usually small & punctures on the skin can be easily identified.

Wound & healing pathophysiology

Acute traumatic wounds are caused by shear, compressive, or tensile forces, which vertically separate the epithelium and dermis.

Shear forces are produced by sharp objects that cut through the skin. The amount of energy required to cut through the skin with a sharp object is relatively low and directed to a very small area
→ little energy is deposited into the surrounding tissue → minimal cell damage. Typically, the resultant wound has straight edges, little contamination, and heals with a good result.

Compressive and tensile forces are produced when a blunt object impacts the skin at right and oblique angles, respectively. In contrast to shear forces, the amount of energy deposited from compressive and tensile injuries is larger
→ disruption of the microvasculature. The devitalized tissue creates an anaerobic environment, which impairs the ability of leukocytes to function and supports
bacterial proliferation. Compressive wounds tend to be stellate or complex, with ragged or shredded edges. Tensile wounds tend to be triangular or produce a flap.

The stages of wound healing are described as: haemostasis, inflammation, epithelialisation, angiogenesis, fibroplasia, contraction, and scar maturation.

Haemostasis is initiated at the time of injury.
- Tissue and vascular smooth muscle contraction → compression of small bleeding vessels.
- Activation of platelets and the coagulation cascade → fibrin clot within the lumens of the severed vessels and within the exposed wound.

Inflammation
- Stimulated by chemotactic factors released by activated platelets and the complement cascade.
- Neutrophils and macrophages phagocytose dead tissue, foreign material, and bacteria, providing physiologic debridement and preventing infection.
- Initially attracts neutrophils followed by macrophages.
  - Neutrophils perform this function for the first 72 hr after injury.
  - Macrophages perform this task for up to 30 days after a traumatic wound.
Epithelialisation reaches a peak about 24 hr after the injury as the inflammatory response stimulates cell division in the stratum basal. Epithelial cells migrate across a closed traumatic wound during the first 24 to 48 h, making the wound impervious to water. Eschar and surface debris impede this process.

Angiogenesis is vital to wound repair. New vessel growth is detectable at 72 hr and peaks in 7-10 days, accounting for the often-marked erythema seen at this time. As the
wound matures vascularity decreases nearly back to baseline at 30 days.

Fibroplasia, with collagen synthesis, reaches a peak by 7 days and essentially replaces the inflammatory mass in the wound by 3 weeks. At the same time of ↑ collagen synthesis, hydrolysis and breakdown of old and damaged collagen is also taking place. At 7-10 days is the vulnerable time when the balance between collagen synthesis and breakdown is most tenuous and unwanted wound separation occurs.

Wound contraction occurs over the next several months. Contraction significantly modifies the cosmetic appearance of treated wounds.

Scar remodeling also occurs over the next several months. Remodeling is such a powerful process that, at the time of suture removal, it is impossible to predict the ultimate appearance of wounds.

Wound management

Triaging wounds

Unless airway and breathing are compromised or there is active bleeding from the wound edge, acute traumatic wounds are evaluated and treated after other life-or limb-threatening conditions have been evaluated and managed.

Haemostasis may be required and is best done by local pressure.

Sometimes, wound repair must be delayed to address other issues. In this case, fresh wounds should be covered by saline-moistened gauze to prevent drying. Encircling clothing, rings, and jewelry should be removed as soon as possible to reduce the potential for damaging
oedema and contamination.

Physical Examination

Neurologic function should be assessed by evaluating distal sensory and motor function.

Absent distal pulses and capillary refill indicate a vascular injury, but their presence does not exclude one.

Tendon function should be performed for each one in isolation, where possible.

Underlying and adjacent structures should be carefully inspected.
Things specific to particular sites:

Areas with excellent vascular supply and a low incidence of infection include the scalp, face, neck, and trunk.
Lacerations on the extremities are at increased risk of infection, and those on the feet and hands are at greatest risk.
Lacerations on the hands can damage tendons, nerves, and joints important for normal function. Lacerations over joints may penetrate into the joint capsule and are at risk for hypertrophic scar formation. Any laceration over the metacarpophalangeal joint is suspicious for a clenched-fist injury.
Lacerations in the perineum have a high likelihood for contamination.

Wound characteristics are important to note.

Large wounds, both in length and width (gaping), are at increased risk of infection.
Wounds with flaps, stellate shape, complex arrangement, avulsed tissue, jagged edges, or deep penetration are at increased risk of infection.
Lacerations heal with best results when the long axis of a laceration is
in the direction of the maximal skin tension.

Wounds that usually require consultation:

Wounds involving the tarsal plate of the eyelid or lacrimal duct.
Wounds involving an open fracture or joint space.
Wounds associated with multiple traumas that need surgical admission.
Wounds of the face that require extensive plastic reconstruction.
Wounds associated with amputation.
Wounds associated with loss of function.
Wounds that involve tendons, nerves, or vessels.
Wounds that involve a significant loss of epidermis.

Types of healing

The three types of clinical wound healing depend on the timing and method by which wound closure is achieved.

Primary closure (healing by primary intention) is performed with sutures, staples, or adhesives at the time of initial evaluation.

Secondary closure (healing by secondary intention) is where the wound is allowed to granulate and fill in with eventual epithelialization with only cleaning and minimal debridement.

Tertiary closure (delayed primary closure) is where the wound is initially cleaned, debrided, and observed for a period of time (typically 4 or 5 days) before closure.

Mode of closure

There are 2 types:

Primary closure - closure of wound by approximation of the wound edges via sutures, staples or skin tape.
Secondary closure - use of non-native tissue (e.g. skin grafts, skin flaps) to achieve closure.

Skin grafts

Skin grafting can provide wound cover in large raw areas that cannot be closed by direct closure.
Skin grafts can be:

Split-thickness skin grafts (STSG) - include two skin layers: the full epidermis and part of the derm.
Full-thickness skin grafts (FTSG) - consists of both the epidermis and complete dermis.

The advantage of STSG includes less tissue use. That offers a higher percentage rate of graft survival and it minimizes the donor site damage.
The one disadvantage, of STSG, is that it tends to contract more than full-thickness skin grafts → poorer cosmetic effect when compared to full-thickness grafts.
Skin should not be grafted over bare bone, tendon, cartilage, major vessels or an irradiated area.

Skin flaps

Skin flaps are an advanced form of skin grafting.
Skin flaps are usually used when the area requiring reconstruction lacks the blood supply needed to support a skin graft. All the tissues that are used to restructure these wounds must carry their own blood supply.
In skin flap surgery, skin, along with underlying fat, blood vessels and sometimes muscle, is moved from a healthy part of the body to the injured site.
Local or distant flaps are preferred to skin grafting if:

the wound bed is not very vascular
bare tendons or nerves are exposed
the wound is over a bony prominence
radiotherapy or repeat surgery is contemplated
better cosmetic effect is required.

References

Burn Survivors Throughout The World, Skin Flaps.
Burn Survivors Throughout The World, Split-Thickness & Full Thickness Grafts.
www.medvarsity.com
Senthil Kumar and David John Leaper, Classification and management of acute wounds, Surgery (Oxford)Volume 26, Issue 2, , Basic skills, February 2008, Pages 43-47. Accessed online.

List of antibodies & autoimmune diseases

2008-02-21T16:16:00.000-08:00

This list is from a handypost by Graham at Over My Med Body!. I'm only duplicating his list below in case his site ever disappears:

Antibody	Disease
Anti-Basement Membrane	Goodpasture’s Syndrome
Anti-Centromere, Anti-Scl 70	Scleroderma (CREST)
Anti-ds DNA	Lupus/SLE
Anti-epithelial cell	Pemphigus Vulgaris
Anti-gliadin	Celiac Disease
Anti-histone	Drug-induced SLE
Anti-IgG, Anti-RF, Anti-CCP	Rheumatoid Arthritis
Antimitochondrial	Primary Biliary Cirrhosis
Anti-neutrophil	Vasculitis
Anti-platelet	ITP
Anti-cholinesterase	Myasthenia Gravis
Anti-endomyesial	Celiac Disease
Anti-Jo 1	poly or dermatomyositis
Anti-SSA, Anti-SSB	Sjögren’s Syndrome

HRT & progesterone

2007-10-09T02:27:00.000-07:00

If you're prescribing HRT to someone, you should also be prescribing progesterone at the same time in the same way that you give laxatives to people on morphine.

(I don't know why - work this out at some stage)

Tutorial - Basic and Applied Anatomy of the Eye

2007-09-12T02:56:00.000-07:00

This site has a great tutorial about opthal stuff. Appears there's a few other things there as well, but I haven't sussed out anything apart from the eye stuff yet.

Hmmm...maybe not

2007-09-02T15:22:00.000-07:00

I just did a Medical Speciality aptitude test that a friend sent me the link for. My results:

Nuclear Medicine - wtf I don't even know the first thing about this!
Infectious diseases - like I know anything about that either!
Plastic Surgery - one of my favourite rotations so far.
Emergency - likewise, another favourite.

Some reflection

2007-09-02T15:01:00.000-07:00

I've just completed the second essay I had to write for this silly portfolio we have to hand in tomorrow. The first essay was infinitely painful - writing up a case report on an ethical issue we had witnessed this year - and I've spent the past few evenings struggle to get that one done.

The second essay I wrote tonight - a reflection of my personal and professional development over this year. It was actually quite cathartic; writing this essay actually felt quite similar to writing a blog entry, so I'm cheating and using it as both. Here goes!!

Third year has been an interesting year; it’s a vastly difference experience to second year. It’s been busier than ever, but despite the busyness it has somehow managed to be less stressful, something I am immensely thankful for, because I am not sure if I could cope with the stress of second year and its barrier exam again. The third year barrier exam that looms in a mere months time somehow does not seem such a daunting task after having been through one before and passed out the other end, and after having successfully made my way through the Long Case exam that was the major stress-inducing object to deal with this year. I’m unsure of whether my reduced stress is due to improved coping, lower motivation to be able to induce stress, or heightened perspective of where I’ve been, where I’m going and what I need to do to get there. Either way, for my sanity’s sake, I am glad.
That’s not to say this year has been a walk in the park. Yes, it’s been very busy, and compared to the last two years, the busyness is less focused and frustrating, because it seems less outcome driven. The year had barely started; our first few days at a new hospital (in Orange) and already we were being bombarded with EBM, PPD and CDT presentations to prepare. Where was the time to study? And what did our lectures have to do with our PBL topics for the week? And what about our ICAs – when were we supposed to learn anything relating to them? And what about the ICAs we never got allocated – will I never learn anything about Respiratory or Neurology?

This year was filled with many unknowns and unanswered questions. I kept waiting for a mystical ah-hah moment, when everything would suddenly snap together and make sense. I continue to wait.

But comparing myself now to where I was at the start of the year, things have changed -just as previous third years, when imparting their wisdom to us - told us they would. Somehow this crazy and confusing system I’ve had to muddle through for the last 7 months has worked. Sure I’m still no pharmacist, but I know a lot more about many more medications than I did this time last year. Flipping through most patients’ medication charts I can make reasonable sense of what their main medical issues are, instead of the bewilderment I felt last year. And sure, I still stammer and give stupid answers whilst in the middle of an operation getting grilled about anatomy by surgeons, but now I welcome it, not dread it, because it’s a great way to learn.

One area I thought I would feel more confident about by this stage is procedural skills. Unfortunately they are something that I continue to feel that if I don’t do them with regularity, then I need to learn again. The only thing I feel vaguely confident in at this stage is venepuncture. Cannulation, ABGs and suturing are still stress inducing experiences for me. I have discussed this with my supervisors, who say don’t get caught up with these things now, that by the time pre-internship arises I’ll be bored with cannulating ten patients a day, that now is the time to be on the wards talking to patients and practicing history-taking and performing physical exams. Taking this advice on board is something I have tried to do, with varying success at times, and is something I am still aware of.

As third year draws to a close, I am stunned by how quickly it has come and gone. I am filled with awe about everything I have learnt this year, and disgust at all that I knew last year but have now forgotten. I’m also starting to think about next year, and all the new experiences that will bring with anticipation. Not to mention the year after.

Anyway, I'm glad that's over and done with. I'm going to go have a glass of wine now, and celebrate its completion, as well as the fact that instead of having a 7:15am vascular tutorial tomorrow morning, we're having it at 2pm instead. I get a sleep-in yay. Much more civilised!! I'm even going to try and go to the gym beforehand as well!

Microalbumuria

2007-08-28T22:47:00.001-07:00

Screening for microalbumuria in non-diabetics is a good way to screen for CV risks. The microalbumuria is caused by endothelial dysfunction.

SAAB drugs for use in acute coronary syndrome

2007-08-28T22:25:00.000-07:00

Statin
Ace inhibitor
Aspirin
Beta blocker

Electrolyte imbalances that occur in diabetes

2007-08-28T18:39:00.000-07:00

Hypocalcaemia - kidney doesn't activate vitamin D -> decreased GIT absorption of Ca
Hyponatraemia
Hyperphosphataemia - it can't be excreted. Treatment is by giving a phosphate binder e.g. mylanta.

Treatment of endocarditis

2007-08-28T17:06:00.000-07:00

Endocarditis requires 6 weeks of IV antibiotic treatment. This length of time is required because it is difficult for antibiotics to penetrate to the valve cusps which are relatively avascular.

Calcium channel blockers

2007-08-23T01:57:00.000-07:00

Mechanism of action

Calcium channel blockers have a negative inotropic effect - they decrease the force of contraction of the myocardium.

They block L-type voltage gated calcium channels in the heart and blood vessels. This prevents calcium levels from increasing as much in the cells when stimulated, leading to less contraction.

They also decrease total peripheral resistance by dilating the blood vessels, and decreasing cardiac output by lowering the force of contraction. Because resistance and output drop, so does blood pressure. With low blood pressure, the heart does not have to work as hard; this can ease problems with cardiomyopathy and coronary disease.

Unlike with beta-blockers, the heart is still responsive to sympathetic nervous system stimulation, so blood pressure can be maintained more effectively.

Many calcium channel blockers also slow down the conduction of electrical activity within the heart by blocking the calcium channel during the plateau phase of the action potential of the heart. This causes a lowering of the heart rate and may cause heart blocks (negative chronotropic effect) of calcium channel blockers.

Classes

There are 2 classes of CCBs:

Dihydropyridines
- Used to reduce systemic vascular resistance and arterial pressure, but are not used to treat angina because the vasodilation and hypotension can lead to reflex tachycardia.
- This CCB class is easily identified by the suffix "-pine" e.g. Amlodepine, Felodipine.

Non-dihydropyridines
- Relatively selective for myocardium, reduce myocardial oxygen demand and reverse coronary vasospasm, and are often used to treat angina.
- They have minimal vasodilatory effects compared with dihydropyridines.
- Action is intracellular.
- E.g. verapamil.

Indications

Atrial fibrillation or flutter - to control heart rate via negative chronotropic effect.

Contraindications

Avoided (or used with caution) in individuals with cardiomyopathy due to negative inotropic effect.
Non-dihydropyridine CCBs should not be combined with beta-blockers because they are both negative inotropes and affect the AV node.

References:

Wikpedia, http://en.wikipedia.org/wiki/Calcium_channel_blocker

Boils, furuncles and impetigo

2007-08-19T20:40:00.000-07:00

Boils (furuncles) are localised, subcutaneous pyogenic infections, most frequently by Staphylococcus aureus, originating deep in a hair follicle.

Impetigo is a contagious superficial pyoderma, caused by Staphylococcus aureus and/or group A streptococci, that begins with a superficial flaccid vesicle that ruptures and forms a thick yellowish crust.

References:

Stedman's Electronic Medical Dictionary, v5.0
Image from http://www.clinical-virology.org/gallery/images/non_viral/impetigo-1.jpg

Wound swabs

2007-08-18T16:56:00.000-07:00

Contamination = the presence of organisms in a wound that are not multiplying.

Colonisation = the presence of organisms in a wound that are multiplying but causing negligible host reaction. Colonisation can have a detrimental effect on wound healing, but as the ‘classic’ signs of infection do not accompany it, is often not identified.

Infection = the presence of organisms in a wound that are multiplying and causing a host reaction.

Signs of infection

delayed healing
purulent discharge from the wound
Green, yellow or brown wound exudate or increased amount of wound exudate
Offensive odour
Inflammation and erythema of the wound and surrounding tissue – may include cellulitis
Hypergranulation tissue
Systemic signs: fever, malaise/lethargy
Increased or unusual pain (Note: persons with diabetes may not experience this)
Confusion
Elevated BSL in diabetics
Leucocytosis

Indications for Wound Swabbing

An obvious wound exists and the surface can be sampled
Clinical signs of infection
Viable tissue exists - not slough or necrotic tissue (although these need to be removed via debridement)

References:

Templeton S., Royal District Nursing Service of SA, http://www.rdns.org.au/research_unit/Newsletters/11_Wound_Sep02.pdf

Chest Imaging tutorial

2007-07-30T02:32:00.000-07:00

Another great radiology resource - this time a tutorial on reading CXRs.

Popliteal fossa

2007-07-26T02:29:00.000-07:00

Boundaries

superior and medial: semitendinosus (semimembranosus is medial to the semitendinosus)
superior and lateral: biceps femoris
inferior and medial: medial head of gastrocnemius
inferior and lateral: lateral head of the gastrocnemius

popliteal artery (continuation of the femoral artery)
popliteal vein
tibial nerve
common peroneal nerve
popliteal lymph nodes embedded in the fat

References

http://en.wikipedia.org/wiki/Popliteal_fossa
Posterior Compartment of the Thigh, http://mywebpages.comcast.net/wnor/postthigh.htm

MedPix™

2007-07-22T17:47:00.000-07:00

MedPix™ is a great radiology resource.

Focal neurological symptoms

2007-07-22T17:38:00.000-07:00

A focal neurologic symptom is a problem that affects either:

A specific location - such as the left face, right farm or even just a small area such as the tongue
A specific function - for example, speech may be affected, but not the ability to write

The problem occurs in the brain or nervous system. The type, location, and severity of the change can indicate the area of the brain or nervous system that is affected.

In contrast, a non-focal problem is NOT specific - such as a general loss of consciousness.

References:

MedLine Plus Medical Encyclopedia, http://www.nlm.nih.gov/medlineplus/ency/article/003191.htm

Asthma Hx

2007-07-22T17:19:00.000-07:00

Things you need to ask someone with asthma:

Sx: wheeze, dyspnoea, cough, disturbed sleep
Exercise - quantify distance to breathlessness
Days per week off work or school
Diurnal variation
Triggers - RTIs, cold, exercise, pets, emotions, drugs
How & when they monitor their asthma e.g. peak flow meter
Use of preventers and inhalers. Has there been any changes?
For elderly people, ask if they've had Fluvax and Pneumovax vaccines (major RF for infective exacerbation)
Any other atopic diseases like eczema, hay fever, allergy
Previous attacks or hospitalisations
Family history of asthma

References:

http://www.aippg.net/forum/viewtopic.php?p=55254

T4 during infection

2007-07-22T17:03:00.000-07:00

Metabolism of thyroid hormones is accelerated during acute infection in man and in experimental animals. The mechanisms for this is uncertain, but activated leukocytes of the infected host have been implicated as potentially important sites of hormone degradation.

Apparently T4 can go up in infection similar to an acute pahse reactant - but I couldn't find anything on the net really backing this up!!

References:

DeRubertis, Accelerated host metabolism of L-thyroxine during acute infection, Journal of Clinical Endocrinology & Metabolism, Vol 40, 589-600

Nilstat

2007-07-22T16:59:00.000-07:00

Actions

Anti-fungal.

Indications

Treatment of candida.

References:

Lipodermatosclerosis (LDS)

2007-07-22T16:48:00.000-07:00

LDS literally means "scarring of the skin and fat" and is a slow process that occurs over a number of years.
Occurs in patients with long-standing venous disease resulting in chronic venous insufficiency.
Affects the skin just above the ankle, usually on the inside surface.
Over time the skin becomes brown, smooth, tight and often painful.
The precise mechanism of LDS is not fully understood, but we do know that it is caused by an excessively high venous pressure in the subcutaneous veins in the lower leg.

References:

http://www.simondodds.com/Venous/LDS.htm
http://www.bu.edu/woundbiotech/wounds/UncommonWounds%20Gallery/pages/19..htm

Chronic Venous Insufficiency (CVI)

2007-07-22T16:32:00.000-07:00

Symptoms

Varicose veins
Ulceration or skin breakdown
Lipodermatosclerosis
Reddened or discolored skin on the leg
Oedema

Risk factors

Heredity
Obesity
Pregnancy
Sedentary lifestyle
Smoking
Jobs requiring long periods of standing or sitting in one place
Age and sex (women in their 50s are more prone to developing CVI)
Incompetent valves
previous DVT

Pathophysiology

Increased venous pressure transcends the venules to the capillaries, impeding flow.
Low-flow states within the capillaries cause leukocyte trapping.
Trapped leukocytes release proteolytic enzymes and oxygen free radicals, which damage capillary basement membranes.
Plasma proteins,such as fibrinogen, leak into the surrounding tissues, forming a fibrin cuff.
Interstitial fibrin and resultant oedema decrease oxygen delivery to the tissues, resulting in local hypoxia.
Inflammation and tissue loss result. Ulceration may occur.

Management

Leg elevation
Elastic compression therapy - especially with older patients you need to ensure they are actually able to put the compression stockings on for themselves.
Sclerotherapy - chemically scarring the veins from the inside out so that they can then no longer fill with blood. Blood that would normally return to the heart through these veins returns to the heart through others. The body eventually absorbs the veins that received the injection.
Vein stripping
Deep vein surgery - note that surgical treatment is reserved for those with discomfort or ulcers refractory to medical management.
Valve repair

Great resource on hands

2007-07-15T02:59:00.000-07:00

Handworld - the name says it all huh? :)

Ankle-Brachial Index

2007-07-14T02:02:00.000-07:00

The Ankle – Brachial Index (ABI) is a ratio of the systolic blood pressure measured simultaneously in the leg and arm. This test is done to screen for peripheral arterial disease (PAD) of the legs.

What the values mean:

An ABI ratio less than 0.8 implies significant arterial obstruction.
A ratio of 0.5 or less implies critical obstruction.
A ratio of < 0.3 implies impending gangrene.

Patients with PAD should not wear compression stockings due to high risk of ischaemia.

References:

Ankle-brachial index test, WebMD
Facts about Intermittent Claudication, North Suburban Cardiology Group

Management of adult cardiorespiratory arresst

2007-07-14T00:58:00.000-07:00

Geris tutorial with the Prof

2007-07-12T04:20:00.000-07:00

The acute geriatric admission

Principle 1 - Atypical presentation

Geriatric giants:

Confusion
Falls
Incontinence
Failure to cope

The reasons that the geriatric syndrome exists and that older people don't present with simple complaints the way younger people would is due to a combination of their underlying medical conditions as well as decreased reserve from multi-system failure and inability to compensate.

Principle 2 - Comorbidity

Multiple Dxes and complex issues in Dx and management plan.
Drugs and bugs - common precipitants of acute hospitalisation.

Principle 3 - Complications of immobility

Seven sins of immobilisation:

pressure sores
constipation and urosepsis
deconditioning
depression
malnutrition
venous thrombosis
bronchopneumonia

Prinicple 4 - Function

Level of function and independence.
Discharge planning on admission.

Rules of prescribing

Rule of halves (impaired drug clearance, increased adverse effects)
Rule of fives (polypharmacy)
Medication untrial (adverse drug reactions)
Medication trial (careful medical management)

Falls

Syncope (Stokes Adams, postural hypotension, aortic stenosis, cerebrovascular disease, epilepsy, diabetic hypoglycaemia SPACED)
Acute - drugs and bugs etc
Chronic - 4 causes: drugs and disorders of eyes, cognition and gait

Incontinence

Post void residual for retention (obstruction or neurological disorder)
5 causes: drugs, UTI, atrophic vaginitis, faecal impaction, prostate

Delirium

Acute and fluctuating, inattention, altered LOC
Reversible causes (drugs and bugs etc)

Giant cell arteritis (GCA)

2007-07-04T03:40:00.000-07:00

Giant cell arteritis is a vasculitis of large and medium size vessels. Although it can affect arteries in the neck, upper body and arms, it occurs most often in the arteries in the temples. For this reason, giant cell arteritis is sometimes called temporal arteritis or cranial arteritis.

Giant cell arteritis is also known as granulomatous arteritis — a reference to a particular type of inflammation it causes.

Epidemiology & Aetiology

Adults older than age 50 are at greatest risk of giant cell arteritis.
Women and caucasians are most commonly affected.
The exact cause isn't known, but researchers believe that genetic, viral and environmental factors may play roles in the inflammation.

Clinical presentation

Giant cell arteritis frequently causes headaches, jaw pain, and blurred or double vision, but the most serious potential complications are blindness and, less often, stroke. These problems occur when swelling in the arteries impairs blood flow to the eyes or brain.

The onset of the symptoms tends to be gradual and includes low grade fever, fatigue, weakness and weight loss.

A new headache, mild or severe, occurs in at least two-thirds of patients with the pain tending to be located over the sides of the head in front of the ears but may be frontal or other located.
Nearly one-half of patients suffer from jaw claudication after chewing.
Impaired vision is often an early manifestation of the disease.
Permanent partial or complete loss of vision in one or both eyes has been observed in 15-20 % of patients. It is rare for patients to become completely blind in both eyes.
Polymyalgia rheumatica, which is characterized by pain in the shoulders and hips, is closely linked to GCA, occurring in about 40-50 % of patients.

Investigations

ESR – elevated in most patients with GCA.
Temporal artery biopsy

Suggested in all cases of suspected GCA even if the diagnosis may appear "classic".
The biopsy is of low risk, causes very little pain, and often leaves little or no scar.
After the use of a topical numbing medication (the same one used by a dentist), a small part of the temporal artery from under the scalp is removed.

Other ways to diagnose GCA include: ultrasonography, angiographic examination, CT scanning and MR angiography, high resolution MRI and position emission tomography (PET).

Management

Although there's no cure for giant cell arteritis, immediate treatment with corticosteroid medications usually relieves symptoms and prevents loss of vision.
Glucocorticoid treatment should be instituted immediately once the diagnosis of GCA is established.
Daily dosing is more effective than alternate day dosing. The response usually occurs within two to four weeks after the institution of therapy.
The diagnosis should be reevaluated in patients who are resistant to adequate steroid therapy.
Steroid withdrawal can begin once clinical remission has been induced.
Relapses are seen more frequently in the first year or two of the disease.
Relapses often necessitate increased dosage or prolonged steroid treatment. Some researchers have suggested that the addition of methotrexate may be steroid-sparing while others have not demonstrated any benefit. However the routine addition of methotrexate to glucocorticoid therapy for GCA is not recommended. The efficacy of other cytotoxic drugs, dapsone, antimalarials, etanercept, and penicillamine has not been studied adequately although they have been reported to be helpful in some case reports.
The finding of an increased risk of visual loss in patients with GCA and thrombocytosis (increase of the number of platelets in the blood), has led some to suggest the addition of drugs like aspirin for patients with high platelet counts, but there is not a lot of data to prove that this may reduce brain/skull problems.

References:

“Giant cell arteritis”, mayoclinic.com, http://www.mayoclinic.com/health/giant-cell-arteritis/DS00440
“Giant Cell Arteritis (Temporal Arteritis)”, Vasculitis Foundation, http://www.vasculitisfoundation.org/giantcellarteritis

Relationship between pulmonary embolism (PE) and atrial fibrillation (AF)

2007-07-04T03:35:00.000-07:00

If PE and AF occur together it is most likely that the PE is the cause of the AF.

The mechanism of the AF is said to be acute right ventricular dilatation with "strain" due to the embolus in the pulmonary circulation creating backpressure into the right ventricle.

If a patient presents with unexplained AF, look for an accompanying PE as the cause.

It is postulated that AF can cause PE if a clot originates in the right atrium rather than the left, but this is less common than clots originating from the right ventricle and more studies need to be done in this area.

References:

Flegel K., When atrial fibrillation occurs with pulmonary embolism, is it the chicken or the egg?, CMAJ 1999;160:1181-2

Tests for hearing loss

2007-05-19T23:44:00.000-07:00

Rinne test

Normal hearing = POSITIVE. Air conduction is louder than bone conduction.
Conductive hearing loss = NEGATIVE. Bone conduction is better than air conduction.
Sensorineural hearing loss = POSITIVE because both bone air and bone conduction are equally reduced (NB: may need to mask normal ear to avoid a false negative from the opposite side).

Weber test

Normal hearing = sound comes from middle of forehead.
Unilateral conductive hearing loss = sound is loudest in AFFECTED ear because the ambient noise is picked up by the normal ear, masking the sound of the tuning fork on that side.
Unilateral sensorineural hearing loss = sound is loudest in UNAFFECTED (normal) ear.

References

http://en.wikipedia.org/wiki/Weber_test
"C:\Tam's docs\uni\Admin\year2\OSCE\Clinical skills summaries\ProcSkills\Procedural Skills.doc"

Sequestra

2007-05-01T05:06:00.000-07:00

A sequestrum is a piece of dead bone that has become separated from normal/sound bone during the process of necrosis . It is a complication (sequelae) of osteomyelitis.

Pathological process of development of sequestra:

infection in the bone -> inflammatory exudate -> increase in intramedullary pressure
periosteum becomes stripped from the osteum -> vascular thrombosis
lack of blood supply -> bone necrosis
sequestra are formed

Due to the avascular nature of sequestra, antibiotics which travel to sites of infection via the bloodstream, poorly penetrate these tissues. Hence the difficulty in treating chronic osteomyelitis.

At the same time as sequestra are developing, new bone is forming (known as involcrum). Openings in the involcrum allow debris and exudates (including pus) to pass from the sequestrum via sinus tracts to the skin.

References:

http://en.wikipedia.org/wiki/Sequestrum

Image from http://www.steinergraphics.com/surgical/006_19.3.html

Stigmata of infective endocarditis

2007-04-30T04:40:00.000-07:00

Fever (often spiking)
Continuous presence of micro-organisms in the bloodstream in serial collection of blood cultures
Vegetations on valves on echocardiography, which sometimes can cause a new or changing heart murmur, particularly murmurs suggestive of valvular regurgitation
Vascular phenomena:

Septic emboli - mitral regurg -> LA dilatation -> ectopic foci -> stasis in LA -> formation of thrombi -> circulatory problems such as stroke or gangrene of fingers
Janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles)
hemorrhage: intracranial hemorrhage, conjunctival hemorrhage, splinter hemorrhages

Immunologic phenomena: Glomerulonephritis, Osler's nodes (painful subcutaneous lesions in the distal fingers), Roth's spots on the retina, positive serum rheumatoid factor

References:

http://en.wikipedia.org/wiki/Endocarditis

Peroneus tendons

2007-04-24T18:36:00.000-07:00

Remember that ligaments are
structures that connect bone to bone wheras tendons are structures that muscle to bone.

The peroneus tendons are often involved in inversion sprains of the ankle if they are overstretched.

The peroneus longus muscle arises from the head and lateral/superior shaft of the fibula. It follows a path down the lateral side of the leg passing behind the lateral malleolus and goes under the lateral aspect of the foot to attach on the plantar surface (bottom) of the foot on the medial cuneiform and the base of the first metatarsal. It performs ankle plantarflexion and eversion.

The peroneus brevis muscle arises from the shaft of the fibular, but more distally on the shaft than peroneus longus. It also passes down the lateral aspect of the lower leg and behind the lateral malleolus to insert on the lateral tubercle of metatarsal V. Unlike peroneus longus, it does not go under the foot. It also performs plantar flexion and eversion of the ankle.

References:

http://www.dubinchiro.com/features/PDF/16ankle.pdf
http://www.courses.vcu.edu/DANC291-003/unit_8.htm

Management of AF

2007-04-24T18:14:00.000-07:00

References:

http://www.aafp.org/afp/20020715/249.html

Difference between a twitch and a tremor

2007-04-24T00:47:00.000-07:00

A twitch is a jerky or spasmodic movement.

A tremor is an involuntary, rhythmical, alternating movement.

Pars defect

2007-04-23T21:44:00.000-07:00

Spondylolysis is a condition in which the there is a defect in a portion of the spine called the pars interarticularis (a small segment of bone joining the facet joints in the back of the spine). The pars interarticularis defect can be on one side of the spine only (unilateral) or both sides (bilateral). The most common level it is found is at L5-S1, although spondylolisthesis can occur at L4-5 and rarely at a higher level.

Spondylolysis is the most common cause of isthmic spondylolisthesis, in which one vertebral body is slipped forward over another.

References:

http://www.spine-health.com/topics/cd/spondy/spondy01.html
http://www.chirogeek.com/005_Spondylo-Slide-Show.htm

Ottawa ankle rules

2007-04-23T21:13:00.000-07:00

Online resources

Wikipedia has a nice, short summary of these rules.
An online version of these rules in also available.

References

http://www.mdcalc.com/anklekneerules

S1Q3T3

2007-04-23T18:37:00.000-07:00

What it is

The S1Q3T3 is the ECG manifestation of acute pressure and volume overload of the right ventricle.

It is characterised by:

Lead I - an S wave signifying a complete or more often incomplete RBBB.
Lead III - a Q wave, slight ST elevation, and an inverted T wave. These findings are due to the pressure and volume overload over the right ventricle which causes repolarization abnormalities.

Causes

Any cause of acute cor pulmonale can cause the S1Q3T3 finding on the ECG. This includes PE, acute bronchospasm, pneumothorax, and other acute lung disorders. In addition, transient LPFB may cause this finding as well.

What this means for Dx'ing PE

The ECG is often abnormal in PE, but findings are not sensitive & not specific. S1Q3T3 pattern is present in only in 20% of cases of PE.

The ECG is a poor diagnostic tool for PE. The greatest utility of the ECG in the patient with suspected PE is ruling out other potential life-threatening diagnoses such as MI.

References:

http://medicine.ucsf.edu/housestaff/Chiefs_cover_sheets/ecg_pe.pdf
http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijem/vol3n1/cor.xml

Ileus

2007-04-16T20:40:00.000-07:00

Ileus is a partial or complete non-mechanical blockage of the small and/or large intestine. It causes colic, vomiting, and constipation.

Ileus occurs because peristalsis stops. Causes of ileus include:

peritonitis
disruption or reduction of the blood supply to the abdomen e.g. post-operatively
kidney diseases, especially when potassium levels are decreased
gallstone ileus - obstruction of the large intestine by a gallstone that has blocked the intestinal opening.

References:

http://www.answers.com/topic/ileus
http://www.answers.com/gallstone%20ileus

Pneumoperitoneum

2007-04-12T16:33:00.000-07:00

Pneumoperitoneum is air or gas in the abdominal (peritoneal) cavity.

A pneumoperitoneum is deliberately created by the surgical team in order to perform laparoscopic surgery. This is achieved by insufflating the abdomen with carbon dioxide.

Aetiology

The most common cause is a perforated abdominal viscus, generally a perforated ulcer, although any part of the bowel may perforate from a benign ulcer, tumor or trauma.

A perforated appendix seldom causes a pneumoperitoneum.

Diagnosis

It is often seen on x-ray, but small amounts are often missed and CT is nowadays regarded as the gold standard in the assessment because CT can visualize as small as 5 cm cubic air.

Complications

Increased intrathoracic pressure -> decreased venous return. This means that DVT prophylaxis is required!!

References:

http://en.wikipedia.org/wiki/Pneumoperitoneum

Reactive arthritis

2007-03-28T01:59:00.000-07:00

Reactive arthritis aka Reiter's syndrome aka Reiter's disease aka arthritis urethritica, venereal arthritis, seronegative spondyloarthropathy, polyarteritis enterica.

Reactive arthritis is a RF-seronegative, HLA-B27-linked spondyloarthropathy with symptoms similar to arthritis or rheumatism. It is caused by genitourinary or gastrointestinal infections, and is thus "reactive", i.e. dependent on the other condition.

Reactive arthritis is the combination of three seemingly unlinked symptoms:

an inflammatory arthritis of large joints
inflammation of the eyes (conjunctivitis and uveitis), and
urethritis.

Epidemiology

Most commonly strikes individuals aged 20-40.
More common in men than in women.
More common in white men than in black men due to white individuals being more likely to have tissue type HLA-B27 than black individuals.
People with HIV have an increased risk of developing reactive arthritis.

History

Reactive arthritis was first described by Hans Reiter, a German military physician, who in 1916 described the disease in a World War I soldier who had recovered from a bout of diarrhea.

The term Reiter's syndrome is being phased out, partly due to a move in the field of medicine to give descriptive names, rather than personal names, to conditions, and partly due to Dr. Reiter's experiments in Nazi concentration camps.

Causes

Reactive arthritis is set off by a preceding infection, the most common of which would be a genital infection with Chlamydia trachomatis.
Other bacteria known to cause reactive arthritis are Neisseria gonorrhoeae, Ureaplasma urealyticum, Salmonella spp., Shigella spp., Yersinia spp., and Campylobacter spp..
A bout of food poisoning or a gastrointestinal infection may also trigger the disease.
Reactive arthritis usually manifests about 1-3 weeks after a known infection.

Pathophysiology

The mechanism of interaction between the infecting organism and the host is unknown.

Synovial fluid cultures are negative, suggesting that RA is caused either by an over-excited autoimmune response or by bacterial antigens which have somehow become deposited in the joints.

Signs and symptoms

Symptoms generally appear within 1-3 weeks but can range from 4-35 days from the onset of the inciting episode of the disease.
The classical presentation is that the first symptom experienced is a urinary symptom such as burning pain on urination (dysuria) or an increased need to urinate (polyuria or frequency).
Other urogenital problems may arise such as prostatitis in men, and cervicitis, salpingitis and/or vulvovaginitis in women.
The arthritis that follows usually affects the large joints such as the knees causing pain and swelling with relative sparing of small joints such as the wrist and hand.
Eye involvement occurs in about 50% of men with urogenital reactive arthritis and about 75% of men with enteric reactive arthritis. Conjunctivitis and uveitis can cause redness of the eyes, eye pain and irritation, and blurred vision.
Roughly 20 to 40 percent of men with reactive arthritis develop penile lesions called balanitis circinata (circinate balanitis) on the end of the penis. A small percentage of men and women develop small hard nodules called keratoderma blennorrhagica on the soles of the feet, and less often on the palms of the hands or elsewhere. In addition, some people develop mouth ulcers that come and go. In some cases, these ulcers are painless and go unnoticed.
About 10 percent of people with Reactive Arthritis, especially those with prolonged disease, will develop cardiac manifestations including aortic regurgitation and pericarditis.

Commonly remembered with the mnemonic "Can't See, Can't Pee, Can't Climb a Tree"

Diagnosis

There are countless clinical symptoms, but the clinical picture is dominated by polyarthritis. There is pain, swelling, redness, and heat in the joints. MRI's are effective for diagnosis.

The urethra, cervix and throat may be swabbed in an attempt to culture the causative organisms. Cultures may be carried out on urine and stool samples.

Synovial fluid from an affected knee may be aspirated to look at the fluid under the microscope and for culture.

A blood test for the gene HLA-B27 may be given to determine if the patient has the gene. About 75 percent of all patients with Reiter's Syndrome have the gene.

Treatment

The main goal of treatment is to identify and eradicate the underlying infectious source with the appropriate antibiotics.
Treatment is symptomatic for each problem. Steroids and analgesics may be given for severe joint inflammation.
Immunosuppressants may be needed for patients with severe reactive arthritis who do not respond to any other treatment.

Prognosis

Reactive arthritis may be self limiting, frequently recurring or develop continually.
Most patients have severe symptoms lasting a few weeks to six months.
Approximately 15 to 50 percent of cases have recurrent bouts of arthritis.
Chronic arthritis or sacroiliitis occurs in 15-30 percent of cases.
Repeated attacks over many years is common, and more than 40 percent of the patients end up with chronic and disabling arthritis, heart disease or impaired vision.
However, most people with reactive arthritis can expect to live normal life spans and maintain a near-normal lifestyle with modest adaptations to protect the involved joints.

References:

http://en.wikipedia.org/wiki/Reiter%27s_disease

Molar pregnancies

2007-03-28T01:00:00.000-07:00

Molar pregnancy aka Hydatidiform mole aka mola hydatidiforma is a common complication of pregnancy, occurring once in every 1000 pregnancies in the US, with much higher rates in Asia (e.g. up to one in 100 pregnancies in Indonesia).

It consists of a nonviable embryo which implants and proliferates within the uterus.

Clinical presentation

Molar pregnancies usually present with painless vaginal bleeding in the fourth to fifth month of preganancy.

Diagnosis

Ultrasound makes the definitive Dx - the uterus may be larger than expected, or the ovaries may be enlarged.
There may also be hyperemesis (more vomiting than would be expected).
Sometimes there is an increase in BP along with proteinuria.
Blood tests will show very high levels of hCG.
Sometimes symptoms of hyperthyroidism are seen, due to the extremely high levels of hCG, which can mimick the normal TSH.

Pathophysiology

A mole is characterized by a conceptus of hyperplastic trophoblastic tissue attached to the placenta. The conceptus does not contain the inner cell mass (the mass of cells inside the primordial embryo that will eventually give rise to the fetus).
The hydatidiform mole can be of two types: a complete mole, in which the abnormal embryonic tissue is derived from the father only; and a partial mole, in which the abnormal tissue is derived from both parents.

Treatment

Hydatidiform moles should be treated by evacuating the uterus by uterine suction or by surgical curettage as soon as possible after diagnosis.
Patients are followed up until their serum hCG titre has fallen to an undetectable level.
Invasive or metastatic moles often respond well to methotrexate. The response to treatment is nearly 100%.
Patients are advised not to conceive for one year after a molar pregnancy.
The chances of having another molar pregnancy are approximately 1%.

References:

http://en.wikipedia.org/wiki/Molar_pregnancy

Ring Blocks

2007-03-19T03:56:00.000-07:00

A digital ring block (aka digital block) is the technique of blocking the nerves of the digits to achieve anesthesia of the finger(s). It is a useful procedure to facilitate minor surgery of the finger.

The nerves to be blocked are the palmar and dorsal digital nerves.

The two palmar nerves supply the anterior aspect of the fingers and are the terminal branches of the median nerve (lateral 3 1/2 fingers) and ulnar nerve (little finger and 1/2 ring finger).

The two dorsal nerves supply the posterior aspect of the fingers and arise from the radial nerve (lateral 2 1/2 to 3 1/2 fingers) and ulna nerve (medial 1 1/2 to 2 1/2 fingers).

If seen in cross section the nerves are at two, five, seven and ten o'clock positions

The procedure:

The patient's hand and fingers are extended and fingers abducted from each other.
The head of the metacarpal bone and base of the proximal phalanx is felt.
The skin is cleaned.
The needle is introduced between the fingers at the point of the interdigital fold and a skin wheal is raised. This is at the level of the head of the metacarpal bone.

The needle is advanced along the axis of the fingers until the palmar aponeurosis is
reached which is felt as a resistance.
Before injection of local anaesthetic the needle must be aspirated to prevent intra-
vascular injection.
1 to 2 mls of local anaesthetic is introduced as the needle is withdrawn.
Subcutaneous injection around the base of the finger is then done through the same skin
wheal to block the palmar and dorsal digital nerves.
The procedure is repeated on the opposite side of the finger.
Massaging the finger after infiltration facilitates spread and increases absorption of the
local anaesthetic.

References:

"Digital Ring Block", Dr. Mary Daniels, Department of Anaesthesia, The Chinese University of Hong Kong, http://sunzi1.lib.hku.hk/hkjo/view/23/2300620.pdf
"Digital Nerve Block", Dr A Hazdic, New York School of Regional Anaesthesia, http://www.nysora.com/techniques/digital_block/

Marcain

2007-03-19T03:48:00.000-07:00

Composition

Bupivacaine hydrochloride +/- Adrenaline

Actions

Bupivacaine is classed as a membrane stabilising agent and is a local anaesthetic of the amide type. Like all amines it causes a reversible blockade of impulse propagation along nerve fibres by preventing the inward movement of sodium ions through the nerve membrane.

Pharmacokinetics

Bupivacaine is a long acting, amide type local anaesthetic chemically related to lignocaine and mepivacaine. It is approximately four times as potent as lignocaine.

References:

MIMS

Indomethacin

2007-03-07T21:31:00.000-08:00

Drug class

NSAID

Action

Potent inhibitor of prostaglandin synthesis. Affords relief of symptoms but does not alter the progressive course of the underlying disease.

Uses

Arthritis and related inflammatory disorders; low back pain; postop bone pain; primary dysmenorrhoea, IBD.

Contraindications

NSAID sensitive asthma; active peptic ulcer, recurrent GI ulceration; pregnancy, lactation

Sold as

Athrexin

Arterial vs venous clots

2007-02-26T02:21:00.000-08:00

Arterial clots

Arteries are thick blood vessels with fast flowing blood. Blood clots in arteries are typically triggered by underlying arteriosclerosis (roughening of the artery wall). Blood platelets get stuck to the roughened blood vessel wall and form a clot. Thus, the medication of choice in trying to prevent thrombosis in arteries are medications that act against platelets. The following medications are anti-platelet drugs:

Aspirin (= ASA)
Plavix (= Clopidogrel)
Ticlid (= Ticlopidine)
Aggrenox (= aspirin plus dipyridamole)

By interfering with platelet function, these drugs increase the patient's risk of bleeding, even though to a lesser degree than coumadin. The INR is not influenced by these drugs and vitamin K intake does not influence their effect.

Venous clots

Veins are thin blood vessels with slow flowing blood. Blood clots that form in veins (DVT, pulmonary embolism) are mainly made up of clotting proteins; platelets do not play a big role in venous clots. Warfarin is an effective anticoagulant by preventing the production of clotting factors in the liver, increasing the INR. It is therefore the drug of choice in venous thrombosis. Anti-platelet drugs do not play much of a role in preventing venous clots.

Occasionally, clots in arteries originate from one of the two left heart chambers and travel from there with the blood stream to the brain, the retina, or the extremities. This typically happens in atrial fibrillation. Such a clot is an arterial embolism that resembles the type of clots seen in veins i.e. they have little platelet participation. They are therefore best treated with warfarin, not with anti-platelet drugs, even though they are clots in arteries.

References:

Thrombophilia Support page

INR & warfarin

2007-02-25T22:11:00.000-08:00

If a patient's INR is > 3 (normal 0.8-1.2) then stop warfarin for a few days rather than reversing it with Vit K/FFPs.

Aneurysms

2007-02-25T20:17:00.000-08:00

An aneurysm is a localized abnormal dilation of a blood vessel or the wall of the heart.

Classification of aortic aneurysms

Aneurysms can be classified by macroscopic shape and size.

Saccular aneurysms are essentially spherical (involving only a portion of the vessel wall) and vary in size from 5 to 20 cm in diameter, often partially or completely filled by thrombus.
Fusiform aneurysms involve a long segment and vary in diameter (up to 20 cm) and length; many involve the entire ascending and transverse portions of the aortic arch, whereas others may involve large segments of the abdominal aorta or even the iliacs.

The shape of an aneurysm is not specific for any disease or clinical manifestations.

Causes of aortic aneurysms

atherosclerosis - causes arterial wall thinning through medial destruction secondary to plaque that originates in the intima.
cystic degeneration of the arterial media
trauma (traumatic aneurysms or arteriovenous aneurysms)
congenital defects such as those causing berry aneurysms (in the brain)
infection resulting in mycotic aneurysms,
systemic diseases e.g. vasculitides

Abdominal aortic aneurysms

Usually positioned below the renal arteries and above the bifurcation of the aorta.
Saccular or fusiform, sometimes up to 15 cm in greatest diameter and of variable length (up to 25 cm).
The aneurysm and the nearby aorta often contain atheromatous ulcers covered by granular mural thrombi, prime sites for the formation of atheroemboli that may lodge in the vessels of the kidneys or lower extremities.
AAAs rarely develop before age 50 and are more common in men.
There is a genetic susceptibility to AAA beyond the genetic predisposition to atherosclerosis or HT.

Aneurysm growth

Most aneurysms expand at a rate of 0.2 to 0.3 cm/year, but 20% expand more rapidly. The most important clinical factor affecting aneurysm growth is blood pressure.

Clinical consequences of AAAs

Rupture into the peritoneal cavity or retroperitoneal tissues with massive, potentially fatal, hemorrhage.
The risk of rupture is directly related to the size of the aneurysm.
Risk varies from zero for a small AAA (less than approximately 4 cm in diameter), to 1% per year for aneurysms measuring 4.0 to 4.9 cm indiameter, 11% per year for aneurysms between 5.0 and 5.9 cm in diameter, and 25% per year for those larger than 6.0 cm.

Obstruction of a vessel, particularly of the iliac, renal, mesenteric, or vertebral branches that supply the spinal cord leading to ischemic tissue injury
Embolism from atheroma or mural thrombus
Impingement on an adjacent structure, such as compression of a ureter or erosion of vertebrae
Presentation as an abdominal mass (often palpably pulsating) that simulates a tumo

Management

Large aneurysms are managed aggressively; operative mortality for unruptured aneurysms is approximately 5%, whereas emergency surgery after rupture carries a mortality rate of more than 50%.

The treatment of abdominal and thoracic aortic aneurysms is evolving toward endoluminal approaches using stent grafts (expandable wire frames covered by a cloth sleeve) rather than surgery for some patients.

Divarication

2007-02-18T16:33:00.000-08:00

The rectus abdominis muscles should meet in the midline at the linea alba. Superior to the umbilicus, some people have a congenital defect that results in a widened linea alba. As a result, when a patient flexes the abdominal muscles the rectus muscles spread apart (divaricate).

Divarication and abdominal hernias appear very similiar. To differentiate between a divarication and a hernia clinically:

get the patient to do a sit-up - rectus muscles spread apart in both a hernia and a divarication
get the patient to cough - rectus muscles will only split apart if its a hernia. When coughing all abdominal muscles are used (not just the rectus), so a divarication will show a diffuse bulging, rather than locally down the midline.

Divarication is common in obese men. It can be surgically corrected, although such an operation would be almost entirely for cosmetic purposes and not of any functional value (unlike a hernia).

Blood flow patterns

2007-02-18T16:16:00.000-08:00

Peripheral muscular arteries always show a triphasic pattern (forward-reverse-forward flow):

forward - steep rise during ventricular systole
reverse - brusque return to baseline with a small negative wave in early diastole caused by the high resistance of small peripheral arteries and capillaries
forward - slow late diastolic rise due to the compliance of the peripheral arterial walls.

A monophasic waveform without the reverse component occurs when the volume in the artery is insufficient and extra flow is required during diastole. This is usually because stenosis or occlusion reduces the blood available to fill the reservoir during systole, but may also occur when there is a large flow to the limb caused by exercise or gross infection.

Neostigmine methylsulfate

2007-02-07T22:45:00.000-08:00

Actions

An anticholinesterase agent which reversibly inhibits the hydrolysis of acetylcholine by competing with acetylcholine for attachment to acetylcholinesterase. As a result, acetylcholine accumulates at cholinergic synapses and its effects are prolonged and exaggerated.
Produces a generalised cholinergic response, including miosis, increased tonus of intestinal and skeletal musculature, constriction of bronchi and ureters, bradycardia and stimulation of salivary and sweat glands.
Used mainly for its direct cholinomimetic effect on skeletal muscle and to a lesser extent to increase the activity of smooth muscle.
Because of its quaternary ammonium structure, neostigmine in moderate doses, does not cross the BBB to produce CNS effects. Extremely high doses, however, produce CNS stimulation followed by CNS depression.

Indications

Reversal of the effects of neuromuscular blocking agents (e.g. tubocurarine, pancuronium).
Prophylaxis and treatment of postoperative intestinal atony and urinary retention.
Treatment of myasthenia gravis during acute exacerbations, when the condition is severe, or in neonates.

Pharmacokinetics

For IV administration the elimination half-life is 47-60 minutes.
For IM administration the elimination half-life is 50-91 minutes.
Approximately 80% of a single IM dose of neostigmine is excreted in the urine in 24 hours, about 50% as unchanged drug and the remainder as metabolites.
The major site of uptake is in the liver. It is metabolised partly by the hydrolysis of the ester linkage and partly by microsomal enzymes in the liver.

Difference between purpura and ecchymoses

2007-01-31T02:44:00.000-08:00

Moved to http://didiaskfor.freehostia.com/index.php?n=CR.AbnormalBleeding

PBL 1 - Structure of synovial joints

2007-01-29T02:21:00.000-08:00

Common postoperative problems

2007-01-28T22:34:00.000-08:00

Postoperative complications are common, despite good pre-op assessment, surgical technique and perioperative management.

Complications can be minimised by regular and close postoperative patient observation. Managing complications effectively requires quick diagnosis and treatment before the complication gets out of hand.

Postoperative pain

Pain from surgical wounds should subside over the first few days, and should be controlled by planned analgesia. Some types of wounds (e.g. vertical abdominal incisions) are more painful than others.
Postoperative pain can be reduced by:
- Preoperative counselling - letting the patient know in advance what to expect after the operation in terms of wounds, IV lines, catheters, extent of pain, plans for pain relief and degree of mobility.
- Peroperative measures - preemptive analgesia to ensure pain does not become established after operation e.g. long acting analgesics, local anaesthetic infiltration into the sound edges, regional nerve blocks, morphine epidurals etc.
- Postoperative analgesia - better to prevent pain than to react to established pain!
Patients vary in their tolerance for pain and need for analgesics. Anxiety, exhaustion and sleep deprivation all reduce pain tolerance.
If the pain is not controlled by what seems to be a normal dose and frequency of analgesia, complications should be suspected.
- Review dose in relation to expected severity of pain and the weight of the patient.
- Consider local postoperative complications such as haematoma -> wound pain, bleeding into fascial compartment -> compartment syndrome, wound infection -> pain increasing after 48 hours.

Pyrexia

Infection is not the only cause of postoperative pyrexia, however it should always be considered and investigated as a cause.
Common postoperative infections include superficial and deep wound infections, chest infections (pneumonia), UTIs and IV cannula site infections.
Infection is not likely to be a cause in fever developing within 2 hours of surgery - it normally takes longer to develop.
Common non-infective causes of pyrexia include transfusion reactions, drug reactions, wound haematomas, DVT and pulmonary emboli.

Tachycardia

Tachycardia can be benign or malignant.
Benign causes of postoperative tachycardia:

pain
anxiety

Malignant causes of postoperative tachycardia:

infection
circulatory disturbances
thyrotoxicosis
Mild tachycardia can be a sign of incipient hypovolaemic shock resulting from haemorrgahe or dehgydration.
Cardiac failure.
AF or flutter.
Anastomotic leakage - after bowel surgery.

Week 2 eve

2007-01-28T04:27:00.000-08:00

Well I've officially been in the OC for just over a week. It feels like a lot longer. My emotions tonight are very different to how I felt sitting here at my desk this time last week.

I'm not really nervous about tomorrow (except about getting grilled about pyloric stenosis). I'm actually looking forward to it, although I'm not looking forward to the 6:30am start. The main thing I'm worried about is mucking up my timetable and inadvertently missing a teaching session in the afternoon. I think the only session I have on is a procedural skills one, but I wouldn't bet my life on it.

I'm hoping that this week I can start working out how to come home at the end of the day and do something productive in the afternoon. The main problem so far is in working out what to do. Let's see how tomorrow goes, one day at a time!

Pyloric stenosis

2007-01-28T04:05:00.000-08:00

Congenital hypertrophic pyloric stenosis

Seen in infants as a disorder that affects males three to four times more often than females, occurring in 1 in 300-900 live births.
Familial occurrence implicates a multifactorial pattern of inheritance; monozygotic twins have a high rate of concordance of the condition.
May occur in association with Turner syndrome, trisomy 18, and esophageal atresia.
The stenosis from hypertrophy, and possibly hyperplasia, of the muscularis propria of the pylorus. Edema and inflammatory changes in the mucosa and submucosa may aggravate the narrowing.

Regurgitation and persistent, projectile, nonbilious vomiting usually appear in the second or third week of life.
Physical examination reveals visible peristalsis and a firm, ovoid palpable mass in the region of the pylorus or distal stomach.
Investigations include barium swallow to look for narrowing, blood tests to check for electrolyte imbalances.
A pyloromyotomy - surgical muscle splitting - is curative.

After surgery, most babies are able to return to normal feedings quickly. The baby starts feeding again 3 to 4 hours after the surgery, and the baby can return to breast-feeding or the formula that he was on prior to the surgery. Because of swelling at the surgery site, the baby may still vomit small amounts for a day or so after surgery. As long as there are no complications, most babies who have undergone pyloromyotomy can return to a normal feeding schedule and be sent home within 48 hours of the surgery.

Acquired pyloric stenosis

Seen in adults.
One of the long-term risks of antral gastritis or peptic ulcers close to the pylorus.
Carcinomas of the pyloric region, lymphomas, or adjacent carcinomas of the pancreas are more ominous causes. In these cases, inflammatory fibrosis or malignant infiltration narrow the pyloric channel, producing pyloric outlet obstruction.
In rare instances, hypertrophic pyloric stenosis is the result of prolonged pyloric spasm.

New kids on the block

2007-01-22T04:24:00.000-08:00

I’ve got absolutely no idea where to start in describing day 1 in hospital. The morning, and indeed most of the day up until 4pm was the usual orientation stuff – getting id issued, hospital tour etc

I’m doing General Surgery for my first rotation, along with another student, who I’ll call Kate here (all names changed to protect the guilty, remember).

At around 4pm myself and Kate paged our registrar to say hello and find out what time we should turn up tomorrow. He asked if we were close by, and when I said we were in the student’s quarters across the road he asked could we meet him in the ED in 5 mins. We were free for the rest of the afternoon, so why not?

The next few hours we were thrown in the deep end taking histories and doing abdominal physical exams of patients in the ED. Although we had just done this stuff last year, I felt so ill-prepared.

Our reg is a lovely, lovely guy, more than a little crazy and I have no doubt that in the next 4 weeks we are going to learn a hell of a lot, and have fun in the process. He is not of the old-school humiliate-your-students-into-learning way of teaching, but will teach us what we are seeing on the day, and expect us to go and learn about it that night, instead of drilling the crap out of us when it’s the first time we are seeing a given case.

Things were off to an eeirily rosy start, right up until we met our consultant. This week is not a good week to get sick because the teams across the state are basically rebuilt from the ground up: brand new interns first week out of uni, new registrars etc. Chaos.

Our reg hadn’t even met his consultant right up until the consultant walked into the room where I was interviewing a patient who presented earlier that day with a palpable mass and right groin pain. Not long after the consultant walked in, our reg walked in. Not long after he walked in, Kate walked in. Our consultant had obviously had enough of people walking in the room, because he then yelled at us all to get out. The reg was mortified and apologized that we had to witness that. He’d never seen anyone act like that before.

Since then he has talked to the consultant who has calmed down and is apparently apologizing to us tomorrow morning. Talk about drama. Let’s see how this unfolds tomorrow!

New beginnings

2007-01-17T22:45:00.000-08:00

The first two years of college are vocabulary lessons.
The second two years are spent learning who to ask and where to look it up.
--Bill Austin

Today was my second day of 3rd year.

Yesterday was spent at uni, in a lecture theatre full of our entire 200-and-something person cohort hearing all about the structure of this year - our rotations, our assessments, how to do Honours, what forms we have to have filled in and hoops we have to have jumped by the end of this year. All this information is summarised in a 70 page handbook. After 6 hours of that, it was all a bit much.

Today was spent at hospital, finding out in more detail where we are expected to be when, what rotations we will be doing, which groups we are in for the different course components, all of which was laid out in a mere 120 pages.

Talk about information overload. I still have no clue exactly what I should and will be doing next week, and I'm still petrified I'll get to the end of this year and realise that I haven't completed some important task such as witnessing an autopsy or performing a PR.

I was alarmed to hear from several speakers that this year is the toughest year of our course. In a lot of ways I feel like I only made it through last year by the skin of my teeth - both in academic terms, and in terms of motivation and sanity. I'm not sure if I have recovered even now.

It's a bit disheartening to hear that even after this year everyone still feels like they are below the curve, despite that fact that this in the year in which we develop most of the clinical skills that will take us through our career. We have been warned finishing this year with big gaps will leave us no future chance to gain the knowledge we missed this year. This is our chance and we need to work our assess off to make the most of it.

In a lot of ways I am exhausted already. I have no idea how I am going to feel next week once this caper gets going properly, let alone 6 months from now when another barrier exam starts looming large.

Today we were encouraged to spend time every day reflecting on what we have seen and learnt in the hospital, and to make a log of it if we can. To remember the patients we see as people, to see the human side of the diseases we learn about. That's how to learn and remember it, how to make it important to us.

Although this is no easy task, that’s why I'm starting this new blog. It's going to be both my log book, and my developmental portfolio.

All names and particulars will be changed to protect both the guilty and the innocent.