file · Web viewAhmad El-Ma'aitaCons 3 – Sheet 19. 24. Management of Pain Emergencies. We will see many patients coming with emergency cases, they need treatment

Alakyaz Assadorian Dr. Ahmad El-Ma'aita Cons 3 – Sheet 19

Management of Pain Emergencies

We will see many patients coming with emergency cases, they need treatment

It has been estimated that 90% of patients coming seeking emergency dental treatment have symptoms of pulpal and/or periapical disease. It is the most common cause of toothache or sometimes headache.

Endodontic emergency treatment usually takes place between regular patients. I.e. these patients are not scheduled so you need to fit them in between your patients, so you need to be very efficient in terms of diagnosing the problem and relieving their symptoms. Diagnostic and therapeutic procedures must be as simple as possible but with the objective of treating the correct tooth and of relieving the patient's pain (we don’t have the luxury to see this patient for one hour so usually you need to relieve their problem within 10-15 minutes maximum which is why it is called "emergency treatment").

Emergency treatment should be the first phase of the regular final treatment. Therefore, whatever you do during this emergency visit shouldn’t jeopardize your final treatment; it should be part of it.

o Sequence of steps to go through;

a- Establish a definitive diagnosis – this is the most important step, the patient came in with pain we need to know what this pain is. We do history and examination until we reach a diagnosis, we can't start our treatment without reaching a diagnosis.

b- Achieve profound anesthesia - if we diagnosed a dental problem and we want to interfere anesthesia! Painful dentistry is not accepted. The patient should not feel any pain (we had a whole lecture concerning anesthesia).

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c- Perform the emergency procedure - we will talk about them, we have many misconceptions here in Jordan and dentistry

d- Prescribe analgesics – most of the times

e- Prescribe antibiotics – sometimes

f- Arrange for definitive appointment

This applies to every single emergency treatment

i. Establish a definitive diagnosis:

- What are the emergencies that may come to our dental practice?

Pain emergencies; below are the most common causes:

1- Dentine hypersensitivity - more common in females mainly because they are more obsessed about oral hygiene.

2- Pulpal inflammation – pulpitis whether reversible or irreversible.3- Acute (symptomatic) apical periodontitis – call it whichever you want, but do not

say acute symptomatic apical periodontitis, it is either acute or symptomatic. 4- Acute apical abscess – very common – patients come with excruciating pain.5- Cracked tooth6- Other oro-facial pain disorders (Non-odontogenic facial pain) – it is common, we

may come across them.

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1- Dentine hypersensitivity: (we will not talk about it too much but it is an important topic)

- Definition: Sharp, short pain arising from exposed dentine in response to stimuli typically thermal, evaporative, tactile, osmotic or chemical and which cannot be ascribed to any other form of dental defect or pathology.

- Aetiology:

Dentine exposure through either:

Loss of enamel: Occlusal wear (attrition), Abrasion, Erosion, Abfraction or Para-functional habits.

Loss of cementum: Gingival recession, Periodontal disease, Root planning, Periodontal surgery.

Theories to explain dentinal hypersensitivity: 1. Odontoblastic transduction theory – weak theory

Odontoblastic processes extend all the way towards the exposed dentine surface and can be excited by a variety of chemical and mechanical stimuli.As a result of such stimulation neurotransmitters are released and impulses are transmitted towards the nerve endings.It is a weak theory because to date no neurotransmitters have been found to be produced or released by Odontoblastic processes, so someone is trying to explain something not much scientific.

2. The neural theory

Nerve fibers present within dentinal tubules initiate impulses when they are injured and cause sensitivity (i.e. direct stimulation of the nerve endings in cases of exposed dentine).

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Against this theory:

Nerve fibers are present only in pre-dentine and inner dentinal zones (they do not extend to the outer part of dentine nearer to the exposure site)

A study has shown that when pain inducing substances like potassium chloride and acetylcholine are applied to exposed dentine, they fail to elicit painful response, therefore this theory has been proven to be weak.

3. The Hydrodynamic theory:

The most widely established and accepted mechanism of action of dentinal hypersensitivity. Proposed by Brannstorm (1972)

This theory postulates that fluids within the dentinal tubules are disturbed either by temperature, physical or osmotic changes and that these fluid changes or movements stimulate a baro-receptor which leads to neural discharge (i.e. fluid movement within the dentinal tubules upon stimulation either by temperature, physical or osmotic changes results in fluid movement and these activate the baroceptors which lead to neural firing and therefore elicit pain).

Differential diagnosis:

We need to differentiate dentinal hypersensitivity from other categories that may elicit the same symptoms as dentinal hypersensitivity:

1. Fractured restoration; leading to dentinal exposure. However, in this case pain

will be more localized, while in dentinal hypersensitivity it is more of a generalized problem; sometimes involving all teeth and sometimes involving a whole quadrant.

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2. Fractured enamel (fractured tooth) exposing dentine – again it is more localized.

3. Dental caries - more localized as well.

4. Post-restoration sensitivity;

Especially common with composite, although until now no scientific evidence has been established to explain the mechanism.

The scenario is; patient comes with no symptoms, receives a composite restoration, and then comes back with symptoms similar to irreversible pulpitis that are very annoying to the patient, but with no enough justification for performing root canal treatment. After removal of the composite, problem is solved.

Most likely explanation is presence of un-polymerized monomers which irritate the pulp, therefore GI / Biodentine other types of liners must be placed prior to filling deep cavities.

5. Cracked tooth syndrome; their vague and poorly localized symptoms could be similar to dentinal hypersensitivity.

6. Bleaching sensitivity; temporary sensitivity especially in the lower anterior teeth.

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Alakyaz Assadorian Dr. Ahmad El-Ma'aita Cons 3 – Sheet 19 Management of dentinal hypersensitivity:

Use of topical agents to cover or plug the exposed dentinal tubules:

Most products available in the market plug the exposed dentinal tubules;

- Calcium – phosphate based products- Fluorides: sodium fluoride (was used in the early generation of

sensodyne, Stannous fluoride- Strontium acetate/ strontium chloride (nowadays used in sensodyne)- Formaldehyde or glutaraldehyde: e.g. Gluma (Glutaraldehyde evaporates

leaving the hydroxyethyl methacrylate particles which plugs the exposed tubules) - Potassium oxalates (used in Crest)- Arginine - Bioactive glass (Novamin)- Dentine adhesives (e.g. varnish)

Depolarization of the nerve fiber endings:

Potassium nitrate – products (used in some sensodyne products); The potassium ion depolarizes the nerve and prevents its re-polarization (prevents nerve stimulation). The nerve impulses do not reach the brain and the resulting pain is stopped.Works gradually over a period of a few weeks!

Placement of restorations:In cases of enamel loss such as Abfraction – you restore with compomer, GIC or composite.

Use of lasers:

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Nd:YAG and CO2Ability to occlude dentinal tubules

Periodontal surgery:

Soft tissue grafting to cover exposed root surfaces (such as in cases of recession which lead to symptoms)e.g.: free gingival grafts (useful), connective tissue grafts and coronally-repositioned flaps.

2- Pulpal inflammation: (Pulpitis can be painful)

We have more established pain in pulpitis;

a. Reversible pulpitis:

- Transient pain of mild to moderate severity - Stimulated pain (not spontaneous); thermal and osmotic sensitivity- Treatment:

Removal of the caries (or cause of the stimulation); sealing of exposed dentineBacteria-tight coronal restoration: either permanent or temporaryA base/ liner might be needed.

b. Irreversible pulpitis:

- Severe dull ache, which lingers upon examination- Spontaneous - but can be made worse by thermal stimulation

(especially hot)

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Alakyaz Assadorian Dr. Ahmad El-Ma'aita Cons 3 – Sheet 19- Poorly localized most of the time, as long as the inflammation had

not spread to the PDL (patient may not be able to differentiate if it is upper or lower, the only thing they know is if it is right or left).

- Diagnosis: Essential to either reproduce the patient's symptoms (palpation, percussion, thermal tests) or relieve the patient's pain (selective anesthesia, cold test)

- Emergency management:

1) Pulp exposure vs. pulpotomy vs. pulp extirpation vs. complete debridementIt is essential to work under aseptic conditions as the pulp is not infected

Pulp exposure; is useless. Most of the time the dentists struggle creating a good access cavity in cases of irreversible pulpitis due to difficult anesthesia, so they just expose the pulp, put some sort of dressing (which we will mention later in this lecture), then wait, hope for the best and prescribe antibiotics for the patient. The pulp will still be in pain until it becomes necrotic. The patient learns to take antibiotics whenever he/she has this same pain – this is one of the bad habits that we need to change, as antibiotics have no role in treating vital teeth.

Pulpotomy; the minimum you can do for a patient with irreversible pulpitis is proper diagnosis, taking good x-rays, anesthetizing and pulpotomy.

Pulp extirpation; we should either do proper extirpation of the pulp or not touch it at all and stop at the pulpotomy stage because the worst thing that can happen to an irreversibly inflamed pulp is to be lacerated.

Complete debridement; if we have time, we can do complete debridement to solve the problem – analgesics may be needed in order to work.

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2) Dressing; definition: is inter-appointment medication!

- Ledermix: is a combination of Demeclocycline hydrochloride (tetracycline) and Triamcinolone acetonide (corticosteroid). We do not have it at JUH but it is very popular worldwide. Some people think it is magic. Sometimes you get osteitis after RCT so if you just put Ledermix it gets you out of jail.

- Non-setting calcium.

- Formocresol??? (Unfortunately we still use it at our clinics. What it does is tissue fixation; however, this is not our objective, we want to get rid of the tissues, not fix them. It has so many disadvantages: it is toxic, mutagenic and carcinogenic).

- None; just leaving some hypochlorite is an option as well.

3) Fluid-tight coronal seal: (MOST IMPORTANT)

The worst thing we can do to our patient is to open an access cavity and leave it open after a case of irreversible pulpitis (where the pulp was vital and sterile); this is a crime!

During placing a temporary filling, keep in mind that;

- There needs to be a good thickness of it; a layer at least 3-4 mm- Maximum 1-2 weeks (do not rely on it for so long)- Different materials can be used; such as:

o ZnO-eugenol-based materials: Cavit, IRM, SuperEBAo Glass ionomer cements o Composite?? If we use composite without bond; it

doesn’t really seal; so it gives you a nice appearance but there is no function in it.

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3- Acute (symptomatic) apical periodontitis:

Presentation:- Tooth painful to chew / touch- Usually well localized pain

Aetiology: - Extension of pulp inflammation- Reaction to pulp necrosis- Trauma or occlusal trauma- Post-endodontic treatment; there are so many steps in root canal

treatment that could lead to tenderness to percussion. In this case, we have to rule out procedural errors such as sodium hypochlorite accidents, over-instrumentation, over-obturation, etc…

Diagnosis:- History - Pulp test; to determine whether the pulp is necrotic and infected or

vital and healthy such as in trauma cases- Occlusal analysis- Radiographic examination

Emergency treatment; depends on aetiology, if:

a- Extension of pulpitis as in management of pulpitis!

b- Reaction to pulp space infection complete debridement + antimicrobial dressing + fluid-tight coronal seal

c- Occlusal trauma occlusal adjustment

d- Post-endodontic treatment exclude endodontic procedural accidents, reassurance, analgesics

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4- Acute apical abscess:

We need to differentiate between Acute Apical Periodontitis and Acute Apical Abscess. AAP is an inflammatory reaction in the periapical tissues, while in AAA the infection inside the tooth is very virulent and severe that it is requiring severe reaction of the body where Neutrophils and leukocytes are all working and producing pus, and this pus is causing swelling, it is entrapped and had not managed its way out, which is why it is called acute.

Presentation: - Severe localized pain that is made worse upon touch or chewing;

most of the times it is localized but fluctuant and sometimes it could be diffuse.

- The tooth in question may feel elevated in the socket (i.e. higher than the other teeth).

- Often associated with swelling (intraoral or extraoral) and systemic signs of infection (trismus, fever, malaise, lymphadenopathy)

Diagnosis: - Presentation- Palpation, percussion, mobility??- Pulp tests- Radiographic examination

Emergency treatment:

- In the rare event of diffusion of the infection to the facial spaces, we need antibiotics with referral to a surgeon since it is a bigger issue than we can handle.

- Most of the times it looks like a swelling; we need to determine the offending tooth.

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- Access cavity; pus may drain through the canal.- Chemo-mechanical instrumentation; proper cleaning of the canals.- If no drainage achieved, create apical patency using sterile size 10 or

15 files- Intra-canal antibacterial dressing (after exudation has stopped)- Coronal seal- Incision and drainage (only if the swelling is fluctuant)

Notes: 1) Incision and drainage is an option, only if we failed to drain the

pus through the canals through creating apical patency. 2) Incision and drainage by itself is NOT a treatment, except if the

tooth is later scheduled for extraction. In this case, incision and drainage is done as an emergency treatment, with antibiotics prescription followed by extraction 3-4 days later.

Leaving the tooth open / open drainage:

- This is a very common practice by so many dentists.- An absolute contraindication for leaving a tooth open is a tooth with

a(n); a) Inflamed vital pulp ORb) Symptomatic apical periodontitis without swelling be left

open for drainage

(Gutmann and Lovdahl, Elsevier 2011)

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- A 5-year retrospective study comprising 2188 patients with necrotic teeth - only 11 teeth were left open because of persistent exudation; so it is not very common.

(Tornstad, Thieme 2003)

Note: If a patient has uncontrolled exudation, we leave the rubber dam on for half an hour then add some dressing. If we open the tooth and leave it open, we will achieve drainage, but the tooth will become infected with all kinds of bacteria. Once we close this tooth, the anaerobic selective environment will be re-established, disturbing the balanced environment that was present when the tooth was left open, leading to a worse problem than what it was before opening the tooth. Therefore, it will be very challenging to treat such a case.

There is clear evidence that the longer a tooth is left open for drainage:

a- The more often apical surgery is required: study compromising 5.000 teeth.- 10.4% were left open, out of these 18% required apical surgery to

manage periapical inflammation (Bence et al., Oral Surg 1980)

b- The more post-op appointments are required to manage the closure of the tooth (Weine et al., Oral Surg 1975)

c- The higher the incidence of flare-ups when closing the tooth for the first time (August J Endod 1982; Bence et al., Oral Surg 1980)

d- The higher the number of intracanal bacteria (Tjaderhance et al., Int Endod J 1995)

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Leaving the tooth open might be considered only in very rare cases when exudation is so severe that it is virtually impossible to close the tooth, and it should be a good clinical practice to re-appoint the patient with 24 hours because the bacteria that has entered inside the canals are still in their planktonic form and are still manageable.

(Rosenberg, Endodontic Topics 2002)

Occlusal reduction:

- Patient has pain to chew/touch.

- There is evidence that: careful reduction of occlusion decreases the incidence of post-operative pain vs. placebo-controlled clinical study (Rosenberg, et al., Endod 1998)

- If the tooth is scheduled to receive cusp-protecting restoration (crown) then occlusal reduction during emergency management is indicated, but not always.

5- Cracked tooth syndrome:

The patient bites, the crack OPENS! The patient still does not feel any pain. The patient keeps biting; saliva and all kinds of fluids enter through the opened crack – there is still no pain. Once the patient lets go, the crack will be compressed and the irritants will compress on the nerve ending of the pulp explaining why sharp quick pain occurs when the patient lets go, but not during biting.

Usually occurs in lower molars.

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Alakyaz Assadorian Dr. Ahmad El-Ma'aita Cons 3 – Sheet 19 Presentation:

- Sharp quick pain upon chewing that is difficult to localize and reproduce

- If the pulp is not affected yet, thermal fluctuations have no influence on pain

Diagnosis:- History- Inspection and detection of cracks (Magnification and Trans-

illumination in order to see the crack)- Dentition status (usually heavily restored / parafunctional habits…)- Pulp tests - Radiographic examination is of little benefit; we do not see anything- Bite test (RD, wedge, tooth sloth)

Emergency management:

a) Without any signs of pulpitis:

In cases where the pulp is healthy, stabilization of the tooth to prevent further progression of the crack is indicated - by means of; orthodontic bands, adhesive restorations (such as composite) or full cuspal coverage (a temporary crown followed by a definitive crown once we make sure no RCT is needed).

b) Pain when not in use (indication of irreversible pulpitis):

In cases where symptoms of pulpitis are present, root canal treatment and cuspal protection are needed.

c) Fracture lines extending below the alveolar crest: Extraction!

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Alakyaz Assadorian Dr. Ahmad El-Ma'aita Cons 3 – Sheet 196- Non-odontogenic facial pain:

Other disorders contributing to toothache or being presented as toothache:

A- Local disorders: jaws, sinuses (sinusitis), salivary glands…

B- Neurological: idiopathic trigeminal neuralgia (sometimes have trigger points near teeth), glossopharyngeal neuralgia, post-herpetic neuralgia, multiple sclerosis.

C- Vascular: migraine, giant cell arteritis, periodic migrainous neuralgia.

D- Psychogenic: chronic idiopathic facial pain (atypical facial pain), burning mouth syndrome, TMD.

E- Referred pain: cardio-respiratory (angina, lung cancer), nasopharyngeal, ocular…

This is probably the only pain category that we reach by exclusion. Therefore if we do not find any dental pathology, we must investigate further and never do any dental treatment.

Emergency management:

- Prescribe analgesics- Refer to a facial pain specialist - DO NOT PERFORM UNNECESSARY DENTAL TREATMENT

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ii. Achieve profound anesthesiaiii. Perform the emergency procedure

iv. Prescribe analgesics:

Broadly classif1- Opioids:

- Not very much used in dentistry because they are not needed. - Some patients specifically ask for them – such as codeine and

pethidine.- Centrally acting! E.g.: Morphine, codeine, pethidine, hydrocodone, oxycodone.

- Advantage: Alleviate pain. - Disadvantages: Lead to addiction, suppress cough and reduce GI

mobility leading to constipation.- E.g.: Co-Codon common analgesic in England; is a combination of

paracetamol and codeine and although it is good but leads to constipation.

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2- Paracetamol (acetaminophen):

- One of the safest and simplest analgesics. - N-acetyl-para-aminophenol (Para-N-acetyl-aminophenol)- Analgesics (mild to moderate pain) and antipyretic- None – very weak anti-inflammatory effect - Mechanism of action is largely unknown. Effect on prostaglandin

synthesis - Side effects and complications:

Generally safe within therapeutic doses (up to 4 gm in 24 hours)Hepato-toxicity is the most serious complication of overdose (>10 gm as a single dose)

- Trade names: Tylenol, Panadol, Revanin…

3- NSAIDs:

Cyclooxygenase enzymes, on which NSAIDs work, are distributed throughout the body and produce prostaglandins (PG-E2, PG-F2Alpha).

COX-1: produce prostaglandins that have protective role for GI lining, regulate platelet function and is necessary for kidney function.

COX-2: produces prostaglandins involved in inflammation and pain.

Inhibition of both enzymes not only alleviates pain and reduces inflammation but also inhibits the protective actions of COX-1 (leading to peptic ulcers).

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Non-selective COX-inhibitors:

a- Ibuprofen:

- Non-selective COX-inhibitor.- Analgesic, antipyretic anti-inflammatory.- Contraindicated: GI ulcers, bleeding disorders, other anticoagulants,

pregnancy (esp. last trimester/ Category D)(Risk of low amniotic fluid level, risk of delayed labour, risk of heart problems for the baby).

- Trade names: Advil, Brufen, Nurofen, Panda.

b- Diclofenac sodium:

- Similar to ibuprofen- Non-selective COX-2 inhibitor- Dose: 50 mg/ 8h (adults)- Trade names: Voltaren, Diclogesic, Cataflam, Zipsor.

c- Naproxen:

- Very Similar to Ibuprofen- Dose: 250 mg/8h- Trade names: NoPain, Proxen, Aleve…

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Selective COX-2 Inhibitors:

Selective inhibition of COX-2 leads to selective pain control with reduced incidence of bleeding, GI and kidney side effects.

Disadvantage: Risk of cardiovascular events; therefore contraindicated in patients with

cardiac disease due to inhibition of COX-2 in blood vessels, which leads to a decrease in the production of prostacyclin in them.

Prostacyclin usually prevents platelet aggregation and vasoconstriction, so its inhibition can lead to excess clot formation and higher blood pressure.

a- Rofecoxib (Vioxx):

- The first selective cox-2 inhibitor.- Was taken off the market in 2004 because the risk of association

with cardiovascular disease was established and patients died.

b- Celecoxib (Celebrex):

- Has a boxed warning on its label; that this medication is actually associated with heart disease.

c- Etericoxib (Arcoxia):

- Approved in more than 80 countries but not the US (since this drug is not approved by the US, then it is not very safe)!

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Note:

We can refer to the "Oxford League Table of Analgesic Efficacy"; that is based on randomized control trials to classify analgesics according to their efficacy.

E.g.:

Ibuprofen 400 mg covers the very top. Therefore, the choice of analgesic should be:

- Ibuprofen 400 mg if not contraindicated OR- Alternating between Ibuprofen 400 mg then 4 hours later

Paracetamol 1000 mg, if the pain is severe.

v. Prescribe antibiotics (IF needed):

All above mentioned pain emergency cases (dentinal hypersensitivity, pulpitis, cracks, non-odontogenic facial pain…) do not require antibiotics. Except for acute apical abscesses with diffuse swelling and systemic involvement such as fever, malaise, lymphadenopathy, trismus, cellulitis, and osteomyelitis.

Notes:

1) We try to restrict the use of antibiotics, to reduce the dangerous "resistance" effect of antibiotics, because we do not want to reach a state where our antibiotics do not work anymore. E.g. of a resistant bacteria is the MRSA which is mostly found in hospitals.

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2) There are too many antibiotics in the market, so we need to have proper antibiotic selection criteria; e.g.: Rodogyl, because it contains subclinical concentrations of metronidazole and spiramycin is the worst/most dangerous thing you can do to a patient.

2003 – Most commonly used antibiotics' efficacy study:

1. Penicillin;- Antibiotic of choice (first line of treatment)!- Advantages: very effective, has low toxicity, targets facultative

anaerobes (which is our target bacteria) and is cheap.- Disadvantage: allergy!

2. Amoxicillin;- Very similar to penicillin, but has a longer half life, a slightly broader

spectrum and is more effective.3. Amoclan (Amoxicillin + Clavulanic Acid);

- Clavulanic acid increases the spectrum of amoxicillin because it works as a beta-lactamase, but is associated with higher risk of developing resistance.

4. Clindamycin;- First alternative choice to penicillin-based antibiotics.- Disadvantage: associated with pseudo-membranous colitis.- No cross allergenicity (unlike cephalosporins).

5. Clarithromycin; - Not commonly used in dentistry.

6. Metronidazole;- Never ever the first choice of treatment for dental infections –

because it is only active against anaerobes but not against aerobes or facultative anaerobes.

- Contraindicated with alcohol. So we need to tell our patients that they cannot consume alcohol when they're on metronidazole because they will have disulfiram-like reaction.

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8 Myths in Prescription of Antibiotics (AAE, colleagues for excellence – Winter 2012):

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Number Myth Fact

1 Antibiotics cure patients Antibiotics do not cure patients

2 Antibiotics are substitutes for surgical intervention

Antibiotics are not substitutes for surgical intervention

3 The most important decision is which antibiotic to use

The most important decision is whether to use one at all

4 Antibiotics increase the host's defense to infection

Antibiotics do not increase the host's defense to infection

5 Multiple antibiotics are superior to a single antibiotic

Multiple antibiotics are not superior to a single antibiotic

6 Bactericidal agents are always superior to bacteriostatic agents

Bactericidal agents are not always superior to bacteriostatic agents

7Antibiotic dosages, dosing intervals

and duration of therapy are established for most infections

Antibiotic dosages, dosing intervals and duration of therapy are not established for most infections

8Bacterial infections require a

"complete course" of antibiotic therapy

Bacterial infections do not require a "complete course" of antibiotic

therapy


Note:

Myth #8 is a debatable issue. They used to say that the patient needs to complete the antibiotics course, but now we say as soon as symptoms are relieved, antibiotics must be stopped.

There is no such thing as a "complete course" of antibiotic therapy. The only guide for determining the effectiveness of antibiotic therapy, and hence, the duration of treatment, is the clinical improvement of the patient. A common misconception asserts that prolonged (after clinical remission of the disease) antibiotic therapy is necessary to prevent "rebound" infections from occurring. Oro-facial infections do not "rebound" if the source of the infection is properly eradicated. Most oro-facial infections persist for two to seven day, and often less. Patients placed on antibiotic therapy for an oro-facial infection should be clinically evaluated on a daily basis. When there is sufficient clinical evidence that the patient's host defenses have regained control of the infection and that the infection is resolving or resolved, the antibiotic therapy should be terminated.

vi. Arrange for definitive treatment

Please refer to the slides for illustrations. Please refer to the article;

www.aae.org/uploadfiles/publications_and_research/endodontics_colleagues_for_excellence_newsletter/ecfewinter12final.pdf

Good luck

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Documents

file · Web viewAhmad El-Ma'aitaCons 3 – Sheet 19. 24. Management of Pain Emergencies. We will see many patients coming with emergency cases, they need treatment