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Tennis Elbow


Pain on the outer part of elbow (lateral epicondyle).

Point tenderness over the lateral epicondyle  a prominent part of the bone on the outside of the elbow.

Gripping and movements of the wrist hurt, especially wrist extension and lifting movements.

Activities that use the muscles that extend the wrist (e.g. pouring a pitcher or gallon of milk, lifting with the palm down) are characteristically painful.

Morning stiffness.


The strongest risk factor for lateral epicondylitis is age. The peak incidence is between 30 to 60 years of age. No difference in incidence between men and women or association between tennis elbow and the dominant hand has been demonstrated.

The pathophysiology of lateral epicondylitis is degenerative. Non-inflammatory, chronic degenerative changes of the origin of the extensor carpi radialis brevis (ECRB) muscle are identified in surgical pathology specimens. It is unclear if the pathology is affected by prior injection of corticosteroid.

Among tennis players, it is believed to be caused by the “repetitive nature of hitting thousands and thousands of tennis balls” which lead to tiny tears in the forearm tendon attachment at the elbow.

The extensor digiti minimi also has a small origin site medial to the elbow which can be affected by this condition. The muscle involves the extension of the fifth digit and some extension of the wrist allowing for adaption to nap or flick the wrist usually associated with a racquet swing. Most often, the extensor muscles become painful due to tendon breakdown from over-extension. Improper form or movement allows for power in a swing to rotate through and around the wrist creating a moment on that joint instead of the elbow joint or rotator cuff. This moment causes pressure to build impact forces to act on the tendon causing irritation and inflammation.

The following speculative rationale is offered by proponents[who?] of an overuse theory of etiology: The extensor carpi radialis brevis has a small origin and does transmit large forces through its tendon during repetitive grasping. It has also been implicated as being vulnerable during shearing stresses during all movements of the forearm.

While it is commonly stated that lateral epicondylitis is caused by repetitive microtrauma/overuse, this is a speculative etiological theory with limited scientific support that is likely overstated. Other speculative risk factors for lateral epicondylitis include taking up tennis later in life, unaccustomed strenuous activity, decreased reaction times and speed and repetitive eccentric muscle contractions (controlled lengthening of a muscle group).

Examination and tests

The diagnosis is made by clinical signs and symptoms, which are usually both discrete and characteristic. There should be point tenderness over the origin of the extensor carpi radialis brevis muscle from the lateral epicondyle (ECRB origin). There should also be pain with passive wrist flexion and also with resisted wrist extension (Cozen’s test), both tested with the elbow extended.

An easy at-home test can be performed to determine whether you have tennis elbow. Stand behind a chair, place your hands on top of the chair back with your palms down, and try to lift the chair up. If this causes pain on the outside of your elbow, the culprit is most likely tennis elbow.

MRI typically shows fluid in the ECRB origin. There may also be a defect in this tissue. The use of the word “tear” to refer to this defect can be misleading. The word “tear” implies injury and the need for repair both of which are probably inaccurate and inappropriate for this degenerative enthesopathy.

Depending on the severity and number of small tendon injuries that build up, the ECRB may not be able to fully heal. Nirschl defined four stages of lateral epicondylitis, showing the introduction of permanent damage beginning at Stage 2. The stages are:

Inflammatory changes that are reversible

Nonreversible pathologic changes to origin of the ECRB muscle

Rupture of ECRB muscle origin

Secondary changes such as fibrosis or calcification


In general the evidence base for intervention measures is poor.

Non-specific palliative treatments include:

Non-steroidal anti-inflammatory drugs (NSAIDs): ibuprofen, naproxen or aspirin

Heat or ice

A counter-force brace or “tennis elbow strap” to reduce strain at the elbow epicondyle, to limit pain provocation and to protect against further damage.

Vibration therapy can be used for localized pain relief and inflammation with vibration therapy devices (Tenease) available for home use.

Rest is the tennis player’s treatment of choice when the pain first appears; the rest allows the tiny tears in the tendon attachment to heal. Tennis players treat more serious cases with ice (although the effectiveness of ice treatment has been challenged in clinical research), anti-inflammatory drugs, soft tissue massage, stretching exercises, and ultrasound therapy.

In recalcitrant cases surgery may be indicated. Many techniques have been described using open, percutaneous or arthroscopic approaches. Most techniques aim to release the strain on the extensor carpi radialis brevis muscle, remove degenerative tissue and promote healing.

Other treatments with limited scientific support include:


Blood injection (possibly augmented by plateletpheresis)

Botulinum toxin

Extra-corporeal shock wave therapy (lithotriptor)

Heat therapy

Immobilization of the forearm and elbow using a splint for two to three weeks

Local injection of cortisone and a numbing medicine

Low level laser therapy

Occupational therapy, primarily for stretching and strengthening of the wrist extensor musculature.

Physical therapy

Platelet-rich plasma

Pulsed ultrasound to break up scar tissue, promote healing, and increase blood flow in the area


Trigger point therapy

There are clinical trials addressing many of these proposed curative treatments, but the quality of these trials is generally poor.

One study has alleged that electrical stimulation combined with acupuncture is beneficial but evaluation studies are inconclusive.

One recent presentation at a scientific meeting described the Tyler Twist Protocol, a physical therapy intervention. Although the study has yet to be published to verify claims made in the newspaper.

Cortisone injections

In four clinical trials comparing corticosteroid injection to placebo (lidocaine) injection that show no effect of the steroids. Complications from repeated steroid injections include skin problems such as hypopigmentation and fat atrophy.

Exercises and stretches

There are several recommendations regarding prevention, treatment, and avoidance of recurrence that are largely speculative including:

Stretches and progressive strengthening exercises to prevent re-irritation of the tendon;

Progressive strengthening involving use of weights or elastic theraband to increase pain free grip strength and forearm strength;

Racquet sport players also are commonly advised to strengthen their shoulder rotator cuff, scapulothoracic and abdominal muscles by Physiotherapists to help reduce any overcompensation in the wrist extensors during gross shoulder and arm movements;

Soft tissue release or simply massage can help reduce the muscular tightness and reduce the tension on the tendons; and

Strapping of the forearm can help realign the muscle fibers and redistribute the load.

Use of a racket designed to dampen the effect of ball striking.

There is little evidence to support the value of these interventions for prevention, treatment, or avoidance of recurrence of lateral epicondylosis.

See also

Golfer’s elbow

Repetitive strain injury

Radial tunnel syndrome


^ Tennis elbow: even cricketers and housewives can get it, a Times of India article dated September 4, 2004

^ a b c What is tennis elbow? from the BBC Sport Academy website

^ Runge F. Zur Genese und Behandlung des Schreibekrampfes. Berliner Klin Wochenschr. 1873;10:245248.

^ Major HP. “Lawn-tennis elbow”. BMJ. 1883;2:557.

^ Kaminsky SB, Baker CL (December 2003). “Lateral epicondylitis of the elbow”. Techniques in Hand & Upper Extremity Surgery 7 (4): 17989. doi:10.1097/00130911-200312000-00009. PMID 16518219. 

^ a b c Boyer MI, Hastings H (1999). “Lateral tennis elbow: “Is there any science out there?””. Journal of Shoulder and Elbow Surgery 8 (5): 48191. doi:10.1016/S1058-2746(99)90081-2. PMID 10543604. 

^ Tennis elbow from the MedlinePlus Medical Encyclopedia

^ from WebMD’s emedicine

^ Bisset L, Paungmali A, Vicenzino B, Beller E (July 2005). “A systematic review and meta-analysis of clinical trials on physical interventions for lateral epicondylalgia”. British Journal of Sports Medicine 39 (7): 41122; discussion 41122. doi:10.1136/bjsm.2004.016170. PMID 15976161. 

^ Pain alleviation by vibratory stimulation, Lundeberg et al, The Journal of Pain, 1984

^ Manias P, Stasinopoulos D (January 2006). “A controlled clinical pilot trial to study the effectiveness of ice as a supplement to the exercise programme for the management of lateral elbow tendinopathy”. British Journal of Sports Medicine 40 (1): 815. doi:10.1136/bjsm.2005.020909. PMID 16371498. 

^ How to treat tennis elbow from the BBC Sport Academy website

^ Lo MY, Safran MR. Surgical treatment of lateral epicondylitis: a systematic review. Clin Orthop Relat Res 2007;463,98-106.

^ Mishra A, Pavelko T (November 2006). “Treatment of chronic elbow tendinosis with buffered platelet-rich plasma”. The American Journal of Sports Medicine 34 (11): 17748. doi:10.1177/0363546506288850. PMID 16735582. 

^ Cowan J, Lozano-Caldern S, Ring D (August 2007). “Quality of prospective controlled randomized trials. Analysis of trials of treatment for lateral epicondylitis as an example”. The Journal of Bone and Joint Surgery 89 (8): 16939. doi:10.2106/JBJS.F.00858. PMID 17671006. 

^ Jiang ZY, Li CD, Guo JH, Li JC, Gao L (November 2005). “[Controlled observation on electroacupuncture combined with cake-separated moxibustion for treatment of tennis elbow]” (in Chinese). Zhongguo Zhen Jiu 25 (11): 7634. PMID 16335198. 

^ New York Times article with video of the Tyler Twist Protocol.

^ Haines T, Stringer B (April 2007). “Corticosteroid injections or physiotherapy were not more effective than wait and see for tennis elbow at 1 year”. Evidence-based Medicine 12 (2): 39. doi:10.1136/ebm.12.2.39. PMID 17400631. 

^ Stasinopoulos D, Stasinopoulou K, Johnson MI (December 2005). “An exercise programme for the management of lateral elbow tendinopathy”. British Journal of Sports Medicine 39 (12): 9447. doi:10.1136/bjsm.2005.019836. PMID 16306504. 

Further reading

Wilson JJ, Best TM (September 2005). “Common overuse tendon problems: A review and recommendations for treatment”. American Family Physician 72 (5): 8118. PMID 16156339. 

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Soft tissue disorders / Rheumatism / Connective tissue arthropathy (M65-M79, 725-727)



Synovitis/Tenosynovitis (Calcific tendinitis, Stenosing tenosynovitis, Trigger finger, DeQuervain’s syndrome)  Transient synovitis  Ganglion cyst

osteochondromatosis (Synovial osteochondromatosis)  Plica syndrome

villonodular synovitis (Giant cell tumor of the tendon sheath)


Bursitis (Olecranon, Prepatellar, Trochanteric, Subacromial)  Synovial cyst (Baker’s cyst)



Fasciitis: Plantar  Nodular  Necrotizing  Eosinophilic


Dupuytren’s contracture  Peyronie’s disease  Plantar fibromatosis  Aggressive fibromatosis  Knuckle pads



upper limb (Adhesive capsulitis of shoulder, Rotator cuff tear, Golfer’s elbow, Tennis elbow)

lower limb (Iliotibial band syndrome, Patellar tendinitis, Achilles tendinitis, Calcaneal spur, Metatarsalgia)  Bone spur

other/general: Tendinitis  Tendinosis

joint navs: anat, non-congenital arthropathies/deformities/dorsopathies/soft tissue arthropathy/congenital, eponymous signs, proc

muscle, DF+DRCT navs: anat/hist/physio, acquired myopathy/congenital myopathy/neoplasia, symptoms+signs/eponymous, proc

v  d  e



Plasma derived mediators

Bradykinin  complement (C3, C5a, MAC)  coagulation (Factor XII, Plasmin, Thrombin)

Cell derived mediators

preformed: Lysosome granules  vasoactive amines (Histamine, Serotonin)

synthesized on demand: cytokines (IFN-, IL-8, TNF-, IL-1)  eicosanoids (Leukotriene B4, Prostaglandins)  Nitric oxide  Kinins


Macrophage  Epithelioid cell  Giant cell  Granuloma


Traditional: Rubor  Calor  Tumor  Dolor (pain)  Functio laesa

Modern: Acute-phase reaction/Fever  Vasodilation  Increased vascular permeability  Exudate  Leukocyte extravasation  Chemotaxis

Specific types


CNS (Encephalitis, Myelitis)  Meningitis (Arachnoiditis)  PNS (Neuritis)  eye (Dacryoadenitis, Scleritis, Keratitis, Choroiditis, Retinitis, Chorioretinitis, Blepharitis, Conjunctivitis, Iritis, Uveitis)  ear (Otitis, Labyrinthitis, Mastoiditis)


Carditis (Endocarditis, Myocarditis, Pericarditis)  Vasculitis (Arteritis, Phlebitis, Capillaritis)


upper (Sinusitis, Rhinitis, Pharyngitis, Laryngitis)  lower (Tracheitis, Bronchitis, Bronchiolitis, Pneumonitis, Pleuritis)  Mediastinitis


mouth (Stomatitis, Gingivitis, Gingivostomatitis, Glossitis, Tonsillitis, Sialadenitis/Parotitis, Cheilitis, Pulpitis, Gnathitis)  tract (Esophagitis, Gastritis, Gastroenteritis, Enteritis, Colitis, Enterocolitis, Duodenitis, Ileitis, Caecitis, Appendicitis, Proctitis)  accessory (Hepatitis, Cholangitis, Cholecystitis, Pancreatitis)  Peritonitis


Dermatitis (Folliculitis)  Cellulitis  Hidradenitis


Arthritis  Dermatomyositis  soft tissue (Myositis, Synovitis/Tenosynovitis, Bursitis, Enthesitis, Fasciitis, Capsulitis, Epicondylitis, Tendinitis, Panniculitis)

Osteochondritis: Osteitis (Spondylitis, Periostitis)  Chondritis


Nephritis (Glomerulonephritis, Pyelonephritis)  Ureteritis  Cystitis  Urethritis


female: Oophoritis  Salpingitis  Endometritis  Parametritis  Cervicitis  Vaginitis  Vulvitis  Mastitis

male: Orchitis  Epididymitis  Prostatitis  Balanitis  Balanoposthitis

pregnancy/newborn: Chorioamnionitis  Omphalitis


Insulitis  Hypophysitis  Thyroiditis  Parathyroiditis  Adrenalitis


Lymphangitis  Lymphadenitis

Categories: Inflammations | Overuse injuries | Tennis terminology | Soft tissue disordersHidden categories: Portal:Tennis/Total | All articles with specifically-marked weasel-worded phrases | Articles with specifically-marked weasel-worded phrases from March 2009
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Acute Abdominal Pain Symptoms

Confused and Scared about a POSSIBLE pregnancy…HELP?

Me and a partner had intercorse earlier this week { by the way: It was protected, no burst in condom, plus no SPERM was released AT ALL}. The female partner went home and stayed up all night into the early hours of the morning. It was 5am when she began to puke and she called me and told me. She, then, had a slight THOUGHT about being pregnant and got very worried. She showed a couple symptoms of pregnancy which were THE SAME EXACT SYMPOTMS of the following: abdominal pain, constipation, diarrhea, FOOD POISONING, gallstones, indigestion, peptic ulcers, UTI’s, vomiting/nausea, chest pain, chronic pain, migranes, HBP, STI {from another partner}, anxiety/panic attacks, depression, stress, possible cervical cancer, endometriosis, menstrual cramps, chronic or acute PID, or a PMS. She’s going to get a pregnancy test today. If anybody has gone through the same or a similar thing and turned out NOT to be pregnant, PLEASE LET US KNOW! WE NEED YOUR HELP!

Well, not to say there isn’t a possibility that she could be pregnant…but you wouldn’t exhibit any signs of pregnancy RIGHT after intercourse unless you were already pregnant prior. A lot of times the stress of thinking you MAY be pregnant can result in similar symptoms. I think it sounds more like the nerves causing some symptoms versus her actually being pregnant ~ especially if there was not a release of sperm. However, if you have had intercourse prior to this one time, you might need to be concerned.

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Acute Abdominal Pain Treatment

ARCALYST® (rilonacept) Meets Primary and All Secondary Endpoints in Phase 3 Trial of Prevention of Gout Flares in …
– Regeneron plans to file by mid-2011 for regulatory approval for ARCALYST in this setting assuming positive results from two ongoing studies read more

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Acute Abdominal Pain Protocol

The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”

“The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”.


Myocardial infarction refers to a dynamic process by which one or more regions of the heart muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood of subsequently, necrosis or death to the myocardial tissue occurs.

The onset of the myocardial infarction process may be sudden or gradual and the progression of the event to complete takes approximately 3 to 6 hours.


Myocardial infarction is the leading cause of death in the United States (US) as well as in most industrialized nations throughout the world. Approximately 800,000 people in the US are affected and in spite of a better awareness of presenting symptoms, 250,000 die prior to presentation to a hospital.4 The survival rate for US patients hospitalized with MI is approximately 90% to 95%. This represents a significant improvement in survival and is related to improvements in emergency medical response and treatment strategies.

In general, MI can occur at any age, but its incidence rises with age. The actual incidence is dependent upon predisposing risk factors for atherosclerosis, which are discussed below. Approximately 50% of all MI’s in the US occur in people younger than 65 years of age. However, in the future, as demographics shift and the mean age of the population increases, a larger percentage of patients presenting with MI will be older than 65 years.

Men are more susceptible than women, but the risk is more in female than in male after menopause.


The coronary arteries supply the capillaries of the myocardium with blood

The right coronary artery (RCA) supplies the right atrium and ventricle, the inferior portion of the left ventricle, the posterior septal wall and the SA and AV nodes

The left coronary artery (LCA) consists of two major branchiate left anterior descending (LAD) and the circumflex (LCX).

The LAD artery supplies below the anterior wall of the left ventricle, anterior ventricular septum and the apex of the left ventricle.

The LCX artery supplies blood to the lateral and posterior surfaces of the left ventricle. 


Levels of cardiac markers rise overtime. Hence, enzymes are drawn in a serial pattern usually on admission and over 6-24 hrs until 3 samples are obtained.

 Enzymes commonly evaluated include CK, CKMB, LDH, TroponinT & I.

 CK-MB ratio indicates the extent of damage of the cardiac muscle. The more the ratio, the more the damage of the cardiac muscle. Troponins are  preferred markers of myocardial injury or they are very cardiac specific & are thought to rise before permanent injury develops.

Increased troponin concentrations should not be used by  themselves to rule out a heart  attack. Troponin will remain high for 1–2 weeks following MI allowing easy diagnosis if patient presents late with an old MI as other CE’s will not be raised unless reinfarction occurs.

Elevation of Cardiac Enzymes in Myocardial Infarction

Enzyme         Rises in        Peaks in      Normalizes in    Normal Value    CKMB ratio

CK                 12 hrs          16-30hrs      3-5 days            35-232IU/L

CKMB            4-8 hrs         24 hrs           72 hrs                < 51IU/L           <6% 

Troponin I    3-6 hrs         20 hrs           14 days              0.0-0.4 ng/ml 

Troponin T    2-4 hrs         8-12 hrs       14 days              0.0-0.1 ng/ml

LDH              12 hrs          12-24 hrs     10 days             100-190 IU/L



The most common sites of MI are in the left ventricle, the chamber of heart which has the greatest work load. Tissue changes that occur in the myocardium are related to the extent to which the cells have been deprived of oxygen. Total deprivation results in an area of infarction in which the cells die and the tissue become necrotic.

Necrosis in this area is evident with in 5 to 6 hours after the occlusion. In response to this necrosis the body increases its products of leukocytes, which aid in the removal of dead cells. As collateral circulation enlarges, it brings fibroblasts, which form a connective tissue scar with in the area of infarction. Usually, the formation of fibrous scar tissue is complete with in 2 to 3 months.

Immediately surrounding the area of infarction is a less seriously damaged area of injury. It may deteriorate and thus extend the area of infarction or with adequate collateral circulation; it may regain its function with in 2 weeks.

The outer most area of damage is the zone of ischemia which borders the area of injury. The cells in this area are weakened by decreased oxygen supply, but function can return usually with in 2 to 3 weeks after the onset of occlusion.


There are two types of risk factors for heart attack, including

  1. Inherited factors
  2. Acquired factors

Inherited factors

These are risk factors you are born with that cannot be changed, but can be improved with medical management and life style changes. Following are most at risk-

  • persons with inherited hypertension
  • persons with inherited low levels of HDL or high levels of LDL
  • persons with a family history of heart disease aging men and women
  • persons with diabetes mellitus [ type 1 diabetes ]
  • women, after the onset of menopause- generally, men are at risk, at an earlier age than women, but after the onset women are equally at risk

Acquired factors

These are risk factors that are caused by activities that we choose to include in our lives that can be managed through life style changes and clinical care. Following are most at risk-

  • Persons with acquired hypertension
  • persons with acquired low level of HDL or high level of LDL
  • cigarette smokers
  • people who are under a lot of stress
  • individual who lives a sedentary life
  • persons overweight by 30 % or more


1.      Different degrees of damage occurs to the heart muscle-

Zone of necrosis: death to the heart muscle caused by extensive and complete oxygen deprivation that is, irreversible damage

Zone of injury: region of heart muscle surrounding the area of necrosis; inflamed and injured, but still viable if adequate oxygen can be restored.

Zone of ischemia: region of the heart muscle surrounding the area of injury, which is ischemic and viable; not endangered unless extension of the infarction occurs.

2.      According to the layers of the heart muscle involved, MI can be classified as-

Transmural or Q wave infarction; area of necrosis occurs throughout the thickness of the heart muscle. Subendocardial or non transmural infarction; area of necrosis is confined to the innermost layer of the heart muscle.

3.      Location of the MI is identified as location of the damaged heart muscle within the left ventricle inferior, anterior, lateral and posterior-

Left ventricle is the most common and dangerous location for MI, as it is the main pumping chamber of the heart

Right ventricular infarction commonly occurs I junction with damage to the inferior and or posterior wall of the left ventricle

4.      Region of the heart muscle that becomes damaged determine by the coronary artery that becomes obstructed

Left main coronary artery

Circumflex branch

Anterior ascending branch

Great cardiac vein

Middle cardiac vein

Right cardiac vein


1)            Chest pain

  • not relieved by the rest over sublingual vasodilator therapy
  • severe steady sub sternal chest pain of a crushing and squeezing nature
  • may radiate to the arms, neck, jaw and shoulders
  • continuous more than 15 minutes
  • may produce anxiety and fear

2)            Diaphoresis

3)            Hypertension or hypotension

4)            Bradycardia or tachycardia

5)            Palpitation, severe anxiety, dyspnea

6)            Disorientation, confusion and restlessness

7)            Fainting, marked weakness

8)            Nausea, vomiting, hiccoughs

9)            Atypical symptoms such as epigastric pain abdominal distress, dull aching or tingling sensation, shortness of breath, extensive fatigue


1.      ECG changes

Generally occur within 2 – 12 hours, but may take 72 – 96 hours.

Necrotic, injured and ischemic tissue alter ventricular depolarization and repolarization

ST segment depression and T wave inversion indicate a pattern of ischemia

ST elevation indicates an injury pattern

  • Anterior small           V3 – V4 leads
  • Anterior extensive    V2 – V5 leads
  • Anteroseptal            V1- V3 leads
  • Posterior                  V1 – V2 leads, progressive R wave and ST depression
  • Anterolateral            V4 – V6, I, Avl leads
  • Apical                        V5 – V6 leads
  • Inferior                     lead ii, iii and avf [ reciprocal ]

2.      Elevation of serum enzymes and isoenzymes:

Enzymes are drawn in a serial pattern usually on admission and every 6 – 24 hours until 3 samples are obtained. Enzyme activity then is correlated to the extent of heart muscle damage

Enzymes commonly evaluated include are CK, LDH, CK-MB, AST, Troponin I, Troponin T. [Fig.4 ]

LDH 2 is normally greater than LDH 1 except when the heart muscle is damaged a reversal occurs

3.      Other findings:

White blood cell count and sedimentation rate elevates due to inflammatory process associated with damaged heart muscle.

Radionuclide imaging allows recognition of areas of decreased perfusion

Position emission tomography determines the presence of reversible heart muscle injury and irreversible or necrotic tissue, extends to which the injured heart muscle has responded to treatment also can be determined


Therapy is aimed at the protection of ischemic and injured heart tissue to preserve muscle function, reduce the infarct size, and prevent death. Innovative modalities provide early restoration of coronary blood flow , and the use of pharmacologic agents improve oxygen supply and demand, reduce and/or prevent disarrhythmias, and inhibit the progression of coronary artery disease.

1.      Opiate analgesic therapy: Morphine is used to relieve pain, improve cardiac hemodynamics by reducing preload and after load and to relieve anxiety.

Meperidine [Demerol] is useful for pain management in those patients contraindicated to morphine or sensitivity to respiratory depression.

2.      Anxiolytic agents: Benzodiazepines are used with analgesics when anxiety complicates chest pain and its relief

3.      Antiplatelet agents: Aspirin interfere with the function of the enzyme cyclooxygenase and inhibits the formation of thromboxane A2. Within minutes aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion

Other antiplatelet agents are, Clopidogrel, Ticlopidine, Dipyridamole, these agents, specifically Clopidogrel may be useful for patients who have a true allergy to aspirin and some times can be used with combination with Aspirin.

4.      Supplemental oxygen: Supplemental oxygen should be administered. The rationale for use is the assurance that erythrocytes will be saturated to maximum carrying capacity. Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and by other tissue may be diminished.

5.      Nitrates: Intravenous Nitrates should be administered in MI, persistent ischemia, hypertension or large anterior wall MI. Nitrates are metabolized to nitric oxide in the vascular endothelium. Nitric oxide relaxes vascular smooth muscle and dilates the blood vessel lumen. Vasodilatation reduces both cardiac preload and after load, and decreases the myocardial oxygen requirements. Vasodilatation of the coronary arteries improves the blood flow through the partially obstructed vessels as well as through collateral vessels. When administered sublingually or intravenously, Nitroglycerin has a rapid onset of action.

6.      Beta adrenergic blocking agents: Beta blockers are recommended within 12 hours of MI symptoms and are continued indefinitely. Beta blockers decrease the rate and force of myocardial contraction and decreases overall myocardial oxygen demand. During the acute phase of MI beta blockers may be initiated intravenously

7.      Heparin: Unfractionated Heparin: intravenous unfractionated Heparin is recommended who undergo percutaneous revascularization. It is also recommended in patients who receive fibrinolytic therapy and non selective fibrinolytic agents such as urokinase, streptokinase and anistreplace. Heparin inhibits the additional formation and propagation of thrombi, effective when administered intravenous or subcutaneously.

Low-molecular-weight-Heparin: can be administered to MI clients not treated with fibrinolytic therapy

8.      Fibrinolytic or Thrombolytic agents: Fibrinolytic therapy is indicated with ST segment elevation. Plasminogen activators restore coronary vessels by dissolving obstructing thrombus. The plasminogen activators have been shown to restore coronary blood flow in 50% to 80% of MI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years. Reteplase has been shown to produce slightly higher 60- and 90-minute angiographic patency rates than accelerated alteplase, while adverse-event rates were equal.

However, the better early patency rate did not translate into any survival advantage at 30 days follow-up. The most critical variable in achieving successful fibrinolysis is time from symptom onset to drug administration. A fibrinolytic is most effective when the “door-to-needle” time is 30 minutes or less.

9.      Angiotensin converting enzyme inhibitors: Oral ACEI are recommended within the first 24 hours of the onset of the MI symptoms, decreases myocardial after load through vasodilatation.

10.  Anti dysarrhythmic agents: Lidocaine decreases ventricular irritability, which commonly occurs post MI.

11.  Calcium channel blockers: Improves the balance between the oxygen supply and demand by decreasing heart rate, blood pressure and dilating coronary vessels.

Diltiazem has been shown to decrease the incidence of reinfarction in patients with non-Q-Wave MIs.

12.  Percutaneous Coronary Intervention [Fig-15]: Mechanical opening of the coronary vessel can be performed during an evolving infarction. A balloon tipped catheter is introduced through a guide wire into a coronary vessel with a non calcified atheromatous lesion. The balloon of the catheter is the inflated, causing disruption of the intima and changes in the atheroma. The result is an increase in the diameter of the lumen of the coronary vessel and improvement of blood flow below the lesion.

Percutaneous coronary intervention is an alternative therapy to fibrinolysis Restoration of coronary blood flow in a MI can be accomplished mechanically by percutaneous coronary intervention (PCI). Mechanical revascularization by PCI is used as a primary therapy as an alternative to fibrinolysis when fibrinolysis is not clearly indicated or contraindicated. PCI can successfully restore coronary blood flow in 90% to 95% of MI patients.

13. Surgical Revascularization: Emergent or urgent coronary artery bypass graft surgery is warranted in the setting of failed percutaneous intervention in patients with hemodynamic instability and coronary anatomy amenable to surgical grafting. Surgical revascularization is also indicated in the setting of mechanical complications of MI such as ventricular septal defect, free wall rupture, or acute mitral regurgitation. Restoration of coronary blood flow with emergency Coronary Artery Bypass Grafting (CABG) can limit myocardial injury and cell death if it is performed within 2 or 3 hours of symptom onset. Emergency CABG carries a higher risk of perioperative morbidity (bleeding and MI extension) and mortality than elective CABG. The risk of operative mortality during emergency CABG is increased in patients, who are in cardiogenic shock, those with previous CABG surgery, and with multi-vessel disease. On the other hand, urgent CABG confers a survival benefit in patients with recurrent ischemia post-MI whose coronary anatomy is unsuitable for complete revascularization with PCI. Elective CABG improves survival in post-MI patients who have left main artery disease, three-vessel disease, or two-vessel disease that is not amenable to PCI. The timing of elective CABG post-MI is controversial, but retrospective studies indicate that when CABG is performed as early as 3 to 7 days post-MI, operative mortality is equivalent to CABG performed on non-MI patients.

14. Cardiac Stress Testing: Cardiac stress testing post-MI has established value in risk stratification and assessment of functional capacity. Stress testing is not recommended within several days post-MI. Only sub-maximal stress tests should be performed in stable patients 4 to 7 days after MI. Exercise testing identifies patients with residual ischemia for additional efforts at revascularization. Exercise testing also provides prognostic information and acts as a guide for post-MI exercise prescription and cardiac rehabilitation.

15. Lipid Management: All post-MI patients should be on an American Heart Association Step II diet (< 200 mg cholesterol/day, < 7% of total calories from saturated fats). Post-MI patients with LDL-cholesterol levels > 100 mg/dL on a Step II diet are recommended to be on drug therapy to lower LDL-cholesterol levels < 100 mg/dL. Post-MI patients with HDL-cholesterol levels < 35 mg/dL on a Step II diet are recommended to participate in a regular exercise program and on drug therapy designed to increase HDL-cholesterol levels.4 Recent data indicate the all MI patients should be on statin therapy, regardless of lipid levels or diet

16. Long-term Medications: Most oral medications instituted in the hospital at the time of MI will be continued long-term. Therapy with aspirin and beta-blockade is continued indefinitely in all patients. ACEI is continued indefinitely in patients with congestive heart failure, left ventricular dysfunction (ejection fraction < 0.40), hypertension, or diabetes. A lipid-lowering agent, specifically a statin, in addition to dietary modification is continued indefinitely 

17. Cardiac Rehabilitation: Cardiac rehabilitation provides a venue for continued education, re-enforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI, which includes exercise training. Participation in cardiac rehabilitation programs post-MI is associated with a decrease in subsequent cardiac morbidity and mortality. Other benefits include improvement in quality of life, functional capacity and social support. A minority of post-MI patients actually participate in formal cardiac rehabilitation programs due to either lack of structured programs, physician referrals, low patient motivation, non-compliance, or financial constraints.


Reperfusion therapy, within which we include thrombolytic therapy and percutaneous coronary intervention (PCI), which includes angioplasty and stent placement, is the greatest advance in the treatment of acute myocardial infarction

Studies have shown that many patients with AMI who are eligible for reperfusion therapy do not receive it. Moreover, of those who do receive it, the time to administration of thrombolytic therapy, or “door-to-needle time” is often delayed, jeopardizing myocardium and leading to greater morbidity and mortality.

 Clinical criteria and simple ECG parameters have limited value for the non-invasive diagnosis of myocardial reperfusion. Other methods, such as ST segment monitoring and kinetic analysis of biochemical markers, may also be value of in early identification of IRA {Infarct Related Artery}, total CK activity, CK-MB isoenzymes appear to be the most promising biochemical markers.

In addition, the thresholds suggested for the diagnosis of reperfusion were generally derived from “time-to-peak” values. This rules out early diagnosis because peak CK plasma values are reached, on averages 9 -+ 6 hours after thrombolysis.

Determination of plasma total and MB CK concentration provides accuracy superior to any other currently available method for the diagnosis of acute MI.

 In addition to providing precise diagnosis of acute MI, quantitative MB CK assays can also be used to obtain an accurate estimate of infarct size. In recent years, accuracy in the diagnosis of acute MI has assumed even greater importance, since the choice and timing of a variety of diagnostic and therapeutic options following coronary care unit admission hinge on whether infarction has occurred. Furthermore, the advent of thrombolytic therapy of acute MI has emphasized the need for more sensitive biochemical markers of necrosis in the first hours. The eventual realization that the reestablishment of blood flow was the dominant mechanism for the diminution of infarct size led to a therapeutic approach dominated by thrombolysis and more literally by the use of interventions to open vessels and maintain them open.

The key observation is that benefit by the use of a drug could be demonstrated if the drug was given prior to the period of ischemia. 

Nevertheless, the greatest benefit in the management of patients with myocardial infarction ha unquestionably been the reestablishment of blood flow as early as possible after occlusion

The aim of this study is to determine the reperfusion of injury exacerbated by thrombolytic drugs in Myocardial Infarction through the process of elevation of cardiac enzymes which peaks and comes to normal levels within 24 hours, preventing prolonged injury and ischemia of myocardial tissue.

However, the aim was to evaluate prospectively biochemical markers for the diagnosis of coronary patency early after IV thrombolysis for Acute Myocardial Infarction.


“The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”.


  • To evaluate the effect of thrombolytic drugs on cardiac enzymes.
  • To compare the effect of thrombolytic drugs and non thrombolytic drugs on cardiac enzymes
  • To determine the importance of thrombolytics for a patient with myocardial infarction
  • To suggest teaching guidelines to public regarding early seeking of medical help at the onset of chest pain.


Effect: Result or produce a result

Thrombolytic drugs: medications used to dissolve blood clots

CPK: A cardiac isoenzyme which releases into the blood in high levels when an injury occurs to the heart. It is also known as Creatine Kinase or Creatine Phophokinase.

CK-MB: It is also a cardiac isoenzyme releases into the blood from the heart muscle during an injury of the heart

Myocardial infarction: Necrosis of a region of the myocardium caused by an interruption in the supply of blood to the heart, usually as a result of occlusion of a coronary artery.


“Thrombolytic agents has effect on fall in peak levels on cardiac enzymes, CK and CK-MB”


Coronary care unit: The data of this research is applicable in the settings of coronary care unit.

Age: Clients are selected only between 35 to 65 yrs of age.

Myocardial infarction: This is also applicable to the clients who were admitted in the hospital within 6 hours of the onset of the chest pain with myocardial infarction who received Inj. Metalyse.

Acute coronary syndrome: The clients who are admitted after 6 hours of the onset of the chest pain with acute coronary syndrome are included in the control group.


This study was done by an experimental method of research design in the settings of Coronary Care Unit in Dubai Hospital, U.A.E. A consecutive series of patients receiving IV Metalyse [ Tenecteplase ]  for MI from May 2006 to November 2006 were included in this study.


This study uses the  comparative design.


This study was conducted in patients irrespective of age, sex and nationality, who were admitted in Coronary Care Unit through Emergency Department in Dubai Hospital, U.A.E.


This study included 60 clients, men and women, irrespective of nationalities, between 35 years to 65 years of age.  Among 60 clients 30 were taken as experimental group and another 30 considered as control group.


The samples are selected as convenient sample, into two groups, the experimental and control groups. The clients who received thrombolytic agents within 6 hours of the onset of the chest pain are selected as an experimental group, and the clients who were presented late after 6 hours of the onset of the chest pain and not received thrombolytics, are selected as control group. All patients treated had the diagnosis of myocardial infarction confirmed by subsequent elevation of both Creatine Kinase [CK] and CK-MB isoenzymes levels. IV Metalyse is administered at a dose of 6000 units to 9000 units according to the weight of the patients. Patients with acute MI who were admitted to CCU more than 6 hours of onset of pain were also included.


Data for the study is collected by an instrument, which consists of 22 items including sample number, age, and sex. Religion, nationality, occupation, food habits, life style onset of chest pain, date and time of admission, signs and symptoms, vital signs, type of MI, protocol of thrombolytic therapy, levels of cardiac enzymes, post thrombolytic treatment, drugs received and date of discharge.

Study reveals that, majority of the clients who had MI was from the Indian subcontinents, constituting 63.3 % and the minority constituting just 1.6 %, from Great Briton and Turkey. 3.3 % of the clients were Egyptians and Syrians. Bangladeshis comprised, 6.6 % and Pakistanis were about 21.6 %. Only 9.9 % of the clients who had MI were Dubai Nationals. Among them 46.6% of the clients were aged between 46 – 55 years and 41.6 % of the clients were between 36 – 45 years and the remaining 11.6 % of the clients are between 56 – 65 years of age.

36.2 % of the clients had acute coronary syndrome and were not given thrombolytics. Remaining of the clients was with true MI and most of them were thrombolysed. However, all clients have undergone coronary angioplasty. Out of these clients only one client had normal coronary vessels, two were with mild coronary stenosis for conservative medical treatment and 4 clients with major triple vessel block were posted for CABG. Rest of the clients was treated with Percutaneous Coronary Angioplasty to LAD [50%], RCA [21.6%] and Circumflex [13.5%].

It is also evident from the study that most of the Indians are affected with MI and the major contributing factors are smoking, stress and lack of knowledge about the disease condition.

Based on Chi-Square deviation the association between normalization of cardiac enzymes levels in the study groups are as follows-

In Experimental group, 30 clients have received Inj. Metalyse . among them except 4 clients, remaining 26 clients reports seen that cardiac enzymes are normalized within 24 hours after the admission and administration of thrombolytic agent.

In control group, 30 clients blood reports for normalization of cardiac enzymes were anlysed, where we found 27 clients reports shown the higher levels of cardiac enzymes after 24 hours of the admission.

  1. Critical Value 14.56,    P value < 0.05 and Null hypothesis rejected

Inj. Metalyse has a good effect on the cardiac muscle provided with Critical Value- 14.56, Probability Value- < 0.05, as evidenced by fall in peak levels of cardiac enzymes CK and CK-MB within 24 hours after received thrombolytic agent.


Tenecteplase [ Metalyse] is a recombinant fibrin-specific plasminogen activator. It binds to the fibrin component of the thrombus and selectively converts thrombus-bound plasminogen to plasmin, which degrades the fibrin matrix of the thrombus. Tenecteplase is cleared from the circulation by binding to specific receptors in the liver followed by catabolism to small peptides.

After single intravenous bolus injection of tenecteplase in patients with acute myocardial infarction, tenecteplase antigen exhibits biphasic elimination from plasma. There is no dose dependence of tenecteplase clearance in the therapeutic dose range.

The initial dominant half-life is 24+_5.5 [mean=/-SD] min. the terminal half-life is 129+_87 minutes, and plasma clearance is 119+_49 ml/min

The main finding of this study is the early peaking of the total CPK level and CK-MB

isoenzymes have identified with successful reperfusion after Metalyse therapy. The peak CPK levels reached in 12 hours and CK-MB levels were shifted in 6 hours. The study reveals that the cardiac enzymes levels peaked and normalized within 24 hours time in the experimental group who received Thrombolytic agents within 6 hours of the onset of the chest pain. Where as it took 3- 5 days for the enzyme levels to peak for clients in the control group, who did not receive thrombolytic agents due to late arrival to the hospital, resulting in more damage to the myocardium.

Thus, it is evident that the extent of injury to the myocardium as well as the oxygen demand is less in the experimental group of the clients. 

Finally, it may be used as a surrogate end point for angiographic demonstration of

patency in future clinical studies of reperfusion therapy. Diagnostic performance improved when the analysis was restricted to patients treated >6 hours after the onset of symptoms.


Clinical studies of fibrinolytic therapy in myocardial infarction show, that early thrombolytic treatment starting within 6 hours of the onset of the chest pain, significantly decreases the risk of further damage of the myocardium and oxygen demand, by the process of fall in peak levels of cardiac enzyme levels within 24 hours.

Inj. Metalyse has early peaking of cardiac enzymes in experimental group reflect the Infarction Related Artery opened, the clot has dissolved by Inj. Metalyse which means we have good thrombolytic effect, that is why we have early peaking levels.

Early identification of patients with persistent occlusion after thrombolyis during

Acute Myocardial Infarction also is important because it can pave the way for rescue interventions such as rescue Percutaneous Transluminal Coronary Angioplasty or repeated thrombolysis.



Determine intensity of client’s angina

Observe for signs and symptoms

Place patient in a comfortable position

Administer oxygen if required

Obtain vital signs every 15 minutes for 2 hours, every half an hour for one hour and

every hour for two hours then as required

Obtain a 12 lead ECG

Monitor for relief of pain

Monitor patient’s response to drug therapy

Institute continuous cardiac monitoring and observe for- reperfusion, arrhythmias, rhythm changes, bradycardia and tachycardia

Interpret rhythm strips

Watch for complaints of headache with use of nitrates

Watch for recurrences of pain. Reinforce the importance of notifying nursing staff whenever pain is experienced.

Administer medications to relieve patient’s anxiety as directed such as sedatives and  tranquilizers

Provide complete bed rest for 24 hours

Determine level of activity that precipitated anginal pain occurs.

Identify specific activities patient may engage in that are below the level at which anginal pain occurs

Prepare for the diagnostic and treatment procedures such as coronary angiogram and PTCA [ Percutaneous Transluminal Coronary Angioplasty]


Counsel on risk factors and life style changes such as-

Methods of stress reduction such as biofeedback and relaxation techniques

Low fat and low cholesterol diet

Avoid excessive caffeine intake

Do not use diet pills, nasal decongestants

Follow up visits to control diabetes and hypertension

Educate patient and family members regarding-

Prevention of recurrence of pain

Regular use of medications

Hazards of smoking

Prevention of other contributing factors

Regular follow up

Importance of dietary modifications

Avoiding activities which cause anginal pain such as sudden exertion, walking against the wind, extremes of temperature, emotionally stressful situations, refraining from engaging in physical activity for 2 hours after meals, reduce weight etc.

Appropriate use of medications

Side effects of medications


Lead interdisciplinary intervention programs

Education of nursing students and staff

Provide in-service nursing education

Maintenance of records and reports

Maintenance of statistics

Making of policies and procedures

Supervision and evaluation of staff performance

Recommendations for further study

A majority of post MI patients actually not participating in formal cardiac rehabilitation programs due to either lack of structured programs, physician

referrals, low patient motivation, non compliance and financial constraints.

Cardiac rehabilitation provides a venue for continued education, reinforcement

of life style modification and adherence to comprehensive prescriptions of

therapies for recovery for MI, which includes exercise training.

Participation in cardiac rehabilitation programs, post MI with a decrease in

subsequent cardiac morbidity and mortality.

Adequate education in the hospitals and work places on causative and contributing factors, preventive measures of heart attacks and re heart attacks, is necessary.

All forms of reperfusion, depending on local facilities, need to be available to patients. Protocols must be written and agreed for the strategy of reperfusion to be applied within a network. Early diagnosis of ST Elevation Myocardial Infarction is essential and is best achieved by rapid ECG recording and interpretation at first medical contact, wherever this contact takes place. 

About the Author

Pushpa Latha, MSN, Vinayaka Missions University, Selam, Madras, India E-Mail Ph- 00971504277926

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Acute Abdominal Pain Women

Acute Appendicitis and Risks For Misdiagnosis and Medical Malpractice

Find out the reasons for and causes of misdiagnosis of appendicitis and how it might present a medical malpractice case and what you can do about it.

The appendix is a small tubular organ attached to the colon. It is located in the lower right quadrant of the abdomen. A blockage within the appendix can be caused by feces, inflammation of intestinal lymph nodes or parasites. An infection of this organ, that serves no function, is potentially life threatening, especially if misdiagnosis occurs.

Patients with abdominal pain make up 5 to 10 percent of emergency room visits. Of those, only a small number will have appendicitis.

Approximately 1.1 in 1,000 people in the US, or 7 percent of the population, will develop appendicitis. The frequency of appendicitis climbs from birth, climaxes at approximately 18 or 19 years and slowly decreases thereafter. Men are almost one and a half times more likely to develop appendicitis than women.

Appendicitis has a high risk for misdiagnosis. There are no conclusive tests for detection of appendicitis. However, there are some procedures which ought to be followed. The physician should apply pressure to the abdomen to check muscle responses and rebound tenderness. A pelvic and/or rectal examination may also be performed. Blood tests are carried out to check for elevated white blood cell counts which may indicate infection. For cases where physical examination and lab tests are inconclusive, CT scans or ultrasound may be utilized.

Symptoms of appendicitis are:

* Rapid onset and worsening of abdominal pain
* Appetite loss
* Nausea or vomiting
* Constipation or diarrhea
* Fever
* Abdominal swelling

Not all patients exhibit these symptoms which leaves open the possibility of misdiagnosis resulting in doctor malpractice.

Another situation that increases the failure to properly diagnose risk is appendicitis can mimic other medical conditions such as:

* Intestinal obstruction
* Inflammatory Bowel Syndrome
* Gynecological disorders
* Intestinal adhesions
* Constipation

Appendicitis is treated by surgical removal of the appendix by either a traditional incision or a laparoscopic procedure. Due to their less invasive nature, Laparatomies generally have less complications and a faster healing rate. If left untreated, the appendix can rupture spilling toxic substances into the abdominal cavity. A perforated appendix increases the morbidity risk substantially.

The mortality rate for appendicitis is 0.2 to 0.8 percent. For patients older than 70, it rises to 20 percent. The perforation rate is higher in people younger than 18 years or older than 50. The mortality and perforation rates may be higher in the last two circumstances due to diagnostic delay.

There are three types of medical misdiagnosis. An improper diagnosis is a diagnosis given based on symptoms that may be similar to another condition. Another kind of misdiagnosis is when a secondary underlying condition is not detected and treated appropriated. The third form is delayed diagnosis where the medical condition is initially overlooked and diagnosis is not made until the condition has worsened.

Misdiagnosis of appendicitis is in the top five medical malpractice categories for lawsuits against emergency room doctors.

Attorney Richard Hastings, for the past two and one half decades, has been helping injured clients and families collect millions of dollars in losses ranging from motor vehicle accidents to wrongful death, to medical malpractice. He is the founder of Selectcounsel, LLC, a free service that helps you find one of the best lawyers in your area and is the author of the books “How To Find A Great Lawyer” and “Understanding And Improving The Value Of Your Personal Injury Case.”

About the Author

Mr. Hastings concentrates his practice on civil and criminal litigation, real estate and business representation.

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