Pantoprazole infusion

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

 

	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

• 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

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

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

• eMedicine: Myocardial Infarction
• How to give thrombolysis in acute myocardial infarction
• eMedicine: Thrombolytic Therapy
• NSW Rural Adult Emergency Clinical Guidelines
• eMJA, Guidelines for the management of acute coronary syndromes 2006

Well’s Criteria for DVT

The Score

1. Active cancer (treatment within last 6 months or palliative) -- 1 point
2. Calf swelling >3 cm compared to other calf (measured 10 cm below tibial tuberosity) -- 1 point
3. Collateral superficial veins (non-varicose) -- 1 point
4. Pitting edema (confined to symptomatic leg) -- 1 point
5. Swelling of entire leg - 1 point
6. Localized pain along distribution of deep venous system—1 point
7. Paralysis, paresis, or recent cast immobilization of lower extremities—1 point
8. Recently bedridden > 3 days, or major surgery requiring regional or general anesthetic in past 4 weeks—1 point
9. 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

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

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

1. 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

2. 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.

3. ECG and occasionally Holter monitoring to detect atrial fibrillation.
4. ECHO cardiogram for persons with suspect underlying cardiac abnormalities.
5. 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

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
  

Wounds

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

1. 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.


2. 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.


3. 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.


4. 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.


5. 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.


6. 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.


7. 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.
   
   
8. 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.
   
   
9. 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.

1. 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.


2. 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.
     
     
3. 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.
   


4. 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.
   


5. 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.
   


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


7. 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.

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


2. 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.
   


3. 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:

1. Primary closure - closure of wound by approximation of the wound edges via sutures, staples or skin tape.
2. 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.
  

Management of adult cardiorespiratory arresst

Peroneus tendons

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

References:

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

Difference between a twitch and a tremor

A twitch is a jerky or spasmodic movement.

A tremor is an involuntary, rhythmical, alternating movement.

Pars defect

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

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

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
  

Reactive arthritis

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:

1. an inflammatory arthritis of large joints
2. inflammation of the eyes (conjunctivitis and uveitis), and
3. 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

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

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/