Shirley ooi emergency medicine pdf

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Guide to essentials in Emergency Medicine 2nd edition Shirley Ooi Emergency Rapid Sequence Intubation: A “How and When To” Guide. Mar 25, eBooks Download Guide to the Essentials in Emergency Medicine (PDF, ePub, Mobi) by Shirley Ooi Online Full Collection. Shirley Ooi is the author of Guide to the Essentials in Emergency Medicine ( avg rating, 37 ratings, 3 reviews, published ), Guide to the Essenti.

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SHIRLEY OOI EMERGENCY MEDICINE PDF - 5 Jun The first edition of the Guide to the Essentials in Emergency Medicine, co-edited by two. Guide to the Essentials in Emergency Medicine by Shirley Ooi, This second edition preserves several of its predecessor's hallmark features. Guide to the Essentials in Emergency Medicine by Shirley Ooi,, available at Book Depository with free delivery worldwide. The first edition of.

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Systemic toxicity is usually dose related and may be organ specific or may have multi organ involvement. General Approach to Management I. Prevention of Absorption III. Enhancement of Elimination IV. Antidotes V. Resuscitation — Airway, Breathing and Circulation Good early supportive care is the key to the management of poisoning. Presence of cough and gag reflexes together with adequate spontaneous ventilation DO NOT warrant endotracheal intubation.

However, when there is concern regarding airway protection and clinical deterioration, it is recommended to secure the airway. Circulation - Patient may present with hypotension or hypertension, bradyarrhythmias or tachyarrhythmias depending on the poison or level of toxicity.

Treatment should be tailored to the most probable cause, however the initial bolus of 1 litre in adult of normal saline is recommended. Inotropic support may be required for refractory hypotension - Hypertension may occur in the setting of sympathomimetic drugs such as amphetamines, ecstasy, methamphetamines ice, crystals , cocaine, anticholinergic, withdrawal from alcohol, nicotine and sedatives.

Treatment of hypertension depends on its chronicity and severity. Hypertensive emergencies evidence of end organ damage require prompt treatment. Intravenous glyceryl trinitrate GTN can be initiated together with close monitoring of the patient blood pressure.

This cocktail is both therapeutic and diagnostic. However, one should beware of the risk of seizures with flumazenil administration. Prevention of Absorption The route of entry for poisons can be dermal, ocular, gastrointestinal or parenteral.

Medical personnel handling the patient MUST at all times adhere to practices using personal protective equipments PPE or standard universal protection.. It involves prolong period of irrigation with normal saline solution and subsequent referral to the ophthalmologist. Caution should be exercised in patients with medical conditions such as bleeding diasthesis and combative patients.

Efficacy which lavage removes gastric contents decreases with time. Insertion of orogastric lavage tube requires special care as known potential complications such as tracheal intubation, esophageal tear, stomach rupture trauma, arrhythmias and aspiration may occur. Stomach content should be retained for analysis.

Whole bowel irrigation is contraindicated in bowel ileus, gastrointestinal bleeding and bowel perforation. Sorbitol is cathartics of choice. Although syrup ipecacuanha is an effective emetic, there is little evidence that its use prevents significant absorption of poisons and therefore rarely use nowadays.

Enhancement of Elimination a. Activated charcoal adsorbs material in the gut, adsorbed drugs are secreted in the bile and binds any drug that diffuses from the circulation into the gut. Multiple-dose Activated Charcoal should be considered in patients who ingested life threatening amount of carbamazepines, dapsone, phenobarbitones, quinine and theophylline.

For carbamates poisoning, supportive therapy together with atropine is adequate. Antidotes - An antidote is a substance that increases the mean lethal dose of a toxin, or that can favorably affect the toxic effect of a poison. Some antidotes are toxic themselves and therefore should be used only when indicated. Common Poisons and Antidotes V. Toxidromes - The term toxidrome refers to constellation of physical signs that can provide clues to narrow the differential diagnosis.

Emergency pdf medicine ooi shirley

However, polydrug or polypharmacy may result in overlapping and confusing mixed syndromes. Toxidromes - A diagnosis of acute poisoning should never be made on the basis of one clinical sign, but there are typical clusters of signs that make a diagnosis of poisoning.

Salicylate Mechanism of Toxicity - Rapidly absorbed from the gastrointestinal tract reaching toxic level within 30 minutes of ingestion. Peak levels may occur in 2 to 4 hours. Simple side-room test for salicylate is feric chloride test which is performed with adding a few drops of FeCI 3 solution to 5 ml of boiled acidified urine.

This will turn violet colour if positive. Pulmonary oedema, cerebral oedema, renal failure, hyperpyrexia, encephalopathy, tetany, hypoglycaemia - Pulmonary oedema is more cardiogenic and is also caused by increased pulmonary capillary permeability.

Hyperventilation causes respiratory alkalosis.


Salicylates induces uncoupling of oxidative phosphorylation and interferes with metabolism and causes accumulation of organic acids. This causes metabolic acidosis.

This is associated with CNS toxicity and a poor prognosis. One value is inadequate for management. Serial values done 6-hourly is necessary. Energetic measures are taken if the patient is ill or deteriorating, whatever the blood level. Monitor prothrombin time PT , platelet count, blod urea and serum electrolytes.

Poisoning with liniment methyl salicylate is commoner than with aspirin in Malaysia. Toxic symptoms correlate poorly with serum levels and initiation of treatment must be based on clinical findings. Approximate serum salicylates level. Poor clinical condition ii. Paracetamol Mechanism of Toxicity - Paracetamol is converted in the liver to a toxic intermediate metabolite NAPQI — N acetyl — p — benzoquinoneimine causing acute centrilobular hepatic necrosis and occasionally acute tubular necrosis.

The toxic intermediate is usually rapidly inactivated by conjugation with reduced gluthathione. Liver damage is maximal 3 — 4 days after ingestion hence liver failure may not be seen until 2 to 3 days later. Toxicity may occur at lower doses i.

Pre-injury period within first 24 hours. Non specific symptoms such as nausea, vomiting, lethargy, malaise and diaphoresis.

Emergency medicine pdf shirley ooi

Patient may also be asymptomatic. Onset of liver injury usually after 24 hours or possibly 12 to 36 hours. Nausea, vomiting, right upper quadrant pain and discomfort. Maximum liver injury occur usually at day 3 or day 4 post ingestion. Symptoms of liver injury such as liver tenderness, jaundice, altered sensorium, easy bruising and even coma.

Guide to the Essentials in Emergency Medicine

Some may develop fulminant liver failure. Recovery period is usually after one week or even longer. It is vital to avoid further injury to liver cells. Specific Management - Resuscitate and stabilize the patients, ensure patent airway and perform definitive airway measure if patient is obtunded or the gag reflex is absent.

Give as Intravenous infusion. If these are present, the infusion should be stopped for 15 minutes and restart at slower rate. Narcotic analgesics Clinical features - Cardio-respiratory - respiratory depression, pulmonary oedema, hypotension, cardiac arrhythmias - Central nervous system — hypothermia, constricted pupils, convulsions, coma - Renal failure Specific Management - IV Naloxone acts almost immediately.

The dosage is IV 0. May be repeated if necessary at 5 minutes and 10 minutes. Close observation is needed because of the very short half life of Naloxone 1 - 2 hours. Watch for return of respiratory depression as the effect of the drug wears off before the opiate effect is over. Naloxone may be given by infusion of 2 mg in ml Normal Saline at a rate adjusted to response. There may be an overreaction with hyperventilation, muscle tremors, tachycardia and hypertension.

The cardinal sign of successful opiate antagonism is an increased respiratory rate and pupil dilatation. The patient may remain drowsy as there is little effect on level of consciousness.

Careful titration of the naloxone dose may prevent this. Recreational drugs These are drugs that being used in the street namely, they are also call as designer drugs.

Therefore, these groups of drugs are call sympathomimetics. Clinical Features - The primary clinical effect is the excitation of the sympathetic nervous system which includes hypertension, tachycardia, mydriasis, diaphoresis, hyperthermia and central nervous system excitation agitation, combative, hallucination, twitching. Specific Management - This includes the management of the complications that may arise from the intoxicated patients. If uncontrolled, it may lead to rhabdomyolysis and life threatening hyperthermia.

Beta blockers is contraindicated in patient with cocaine abuse because of the paradoxical hypertension, when the primary cause of cocaine induced vasoconstriction is untreated and unopposed.

This is when the etiology of wide complex tachycardia from cocaine is unknown. Treatment for myocardial ischaemia or infarction induce by cocaine is similar to those not induce by cocaine. Management include crush aspirin mg, heparin, nitrates either given sublingual or intravenous, sedation with benzodiazepines, and morphine for analgesic properties.

They often swallowed large numbers of packages with each containing a potentially fatal dose of drug. Endoscopy and induce emesis, but these are potentially dangerous b. Use Sorbitol or Lactulose to increase bowel transit time. Common agents that are smuggled through this method are: Pesticides 5a. Organophosphorous compounds I.

Organophosphate II. Carbamates 5b. Paraquat 5a. Clinical Features Present with classical cholinergic syndromes, manifested by hyperactivity of cholinergic responses at receptors sites causing SLUDGE Syndrome Hallmark features are miosis, bradycardia, excessive salivation and muscle twitching and fasciculation may appear within few minutes to 12 hours after exposure. Rehydrate the patients to avoid circulatory compromised. The doses must be titrated to achieve adequate atropinisation. Adequate atropinisation indicated by complete clearing of rales and drying of pulmonary secretions.

The patient should be kept well atropinised for at least 5 — 7 days. Continue for 24 — 48 hours depend upon clinical response and serum cholinesterase levels. Phenytoin may be also be used for frequent seizures. Carbamates Mechanism of Toxicity - Inhibition of acetylcholinesterase at the esteric sites on the enzymes molecules. The chemical bond is much more labile minutes to hours than that characterizing the phosphorylation by organophosphate insecticides.

Paraquat Mechanism of Toxicity - Paraquat is reduced in biologic tissues to free radicals, which react with oxygen to form superoxide and hydrogen peroxide which is thought to induce tissue damage. Death often results from pulmonary oedema.

This is a very toxic agent and it is essential that its absorption should be prevented. Treatment must be started at the earliest opportunity.

During the 2 nd week, pulmonary fibrosis and oedema occurs due to selective accumulation of paraquat in lung tissues. No oxygen as this tends to increase the toxic effects on the lungs. Methanol Mechanism of Toxicity - Toxicity is seen in consumption of adulterated alcohol and denatured ethanol. Methanol is a common solvent.

Methanol is oxidized by alcohol dehydrogenase first to formaldehyde and then to formic acid. Alcohol dehydrogenase has a much higher affinity for ethanol and hence ethanol is used to competitively inhibit the metabolism of methanol.

Specific Management - Gastric lavage if less than one hours of ingestion. Large amounts may be necessary. Return of acidosis is frequent after initial dose and additional alkali may be required. The duration of anticoagulant effect is up to 7 days. Provide fluid for volume replacement to avoid circulatory compromised - Perform gastric lavage if ingestion occurs within one hour. If bleeding, give FFP. Pulmonary damage is manifested as pulmonary oedema or pneumonitis.

Death is from respiratory depression. When large amounts are ingested, coma with respiratory depression may occur. Clinical Features - Patient may initially have mild symptoms and then develop difficulty in breathing, bronchospasm, wheezing, rales and fever within 6 hours.

Alteration in mental state is a sign of hypoxia or hypercapnia.

The low surface tension of petroleum distillate allows minute amounts to spread widely throughout the lungs, producing pulmonary oedema or pneumonitis. Pulmonary damage may also arise from absorption of ingested petroleum distillates. Specific Management - Be extremely careful to prevent aspiration.

Coughing is a bad sign indicating aspiration. Carbon monoxide Mechanism of Toxicity - Carbon monoxide is a clear colourless and odorless gas. The mechanisms of carbon monoxide CO toxicities are not fully understood. The binding affinity of CO to haemoglobin is times than that of oxygen, therefore impairing the delivery of oxygen to the tissue.

This will cause profound tissue hypoxia. CO also binds to myoglobin, resulting in worsening of the hypoxia in cardiac muscle, and to the mitochondrial cytochrome oxydase, causing impairment of ATP production. Clinical Features - Acute exposure leads to multisystem signs and symptoms. Sign of neurological injury may persist from time of poisoning till after 2 to 21 days. Dyspnoea dan hyperpnoea, bronchopneumonia and non cardiogenic pulmonaty oedema - Cardiovascular: Oxygen therapy speed the elimination of CO from the body.

Without therapy, the elimination half life of CO is 4 to 5 hours. However, patient should seek treatment if there is respiratory, cardiovascular or neurological symptoms. Patient should be asked to refrain from smoking for at least 72 hours. If in doubt, admit patient for observation. Sedative hypnotics A broad range of drugs fall under this group. Common ones are benzodiazepines and barbiturates. In general, the toxic effect is depression of the central nervous system. Clinical manifestations - Nystamus, ataxia, dysarthria, somnolence, respiratory depression, hypotension, hyporthermia and coma.

Cathartics may be considered. Flumazenil have short half life therefore repeated doses may be required. However, flumazenil is contraindicated if: Caution for withdrawal symptoms for abrupt cessation of benzodiazepines Phenobarbitone 60 - Mild toxicity cause drowsiness, slurred speech, ataxia, unsteady gait, nystagmus, emotional lability and impaired cognition. Severe intoxication leads to coma and respiratory arrest. Supportive care especially to cardiovascular and respiratory.

Multidoses of activated charcoal will hasten elimination, given as 50gm in water. Repeat if necessary. Consider haemodialysis in severe poisoning when involve renal or cardiac failure, acid base or electrolytes abnormalities Table Caustics - Caustic agents are diverse group of substance that have the potential to cause tissue burns on contact with gastrointestinal tract, upper and lower airways, eye, and skin.

These agents frequently used as part of the formulation for household cleaning product such as toilet bowl cleaner, floor detergents, rust remover, drain cleaner, oven cleaner, dishwashing detergents and many more. Mechanism of Toxicity - The effect of the caustic can be minimal to invariably fatal, based on the agent, the amount ingested, the concentrations of the agents, the duration of exposure and the route of exposure, and whether there is presence or absence of food in the stomach.

When strong acid in contact with the epithelium, a coagulum or eschar is created, limiting further spread of the acid. Clinical Features - Clinical features are due to direct contact to the victims mucosal area.

Small ingestions of potent ot highly concentrated caustic agents can be as serious as larger ingestions. In severe cases it involves symptoms of upper and lower airway compromise such as coughing, wheezing, throat pain, stridor and dysphonia. This is due to an airway irritations and oedema. Victims also may complain of abdominal pain and this may be due to hollow viscus perforation or extension of the burn injury to the adjoining visceral areas. Specific Management - The goal of treatment is to identify the extend and severity of the burn injury.

References Chapter 11 Poisonous snake bites Table of contents 1. Specific snake bites A. Hydrophidae Sea Snakes C. Viperidae Pit Viper 3. Specific treatment of venomous snake bites 1. Introduction - Venomous snake bite - Snake bites remains an important cause of mortality and morbidity in developing countries. It is estimated that up to , people annually die of snake bite world wide. Of these, 18 species of land and all 22 species of sea snakes are venomous. There 3 main types of venomous snakes in Malaysia A.

Elapidae Cobras B. Viperidae Vipers 2. Cobra, kraits, coral and sea snakes are the main species in this family. Cobra bites are painful and accompanied by slow local swelling, necrosis and later wet gangrene. There is no or minimal pain with other elapids. The venom is predominantly neurotoxic. Cardiovascular depression is seen in severe poisoning. Onset may be delayed for up to 10 hours.

In severe poisoning, the patient is unable to speak, cough, swallow, protrude his tongue or move the jaw. Sea snakes are recognizable by having flat tail like a blade. The effect is exclusively systemic.

The venom is both myotoxic and neurotoxic. Tendon reflexes may be depressed. Neurotoxic effect also include ptosis, trismus and blurring of vision. Respiratory failure may occur within a few hours to 60 hours after the bite.

The commonest species found in Malaysia is Malayan pit viper. Predominantly vasculotoxic with rapid swelling of the bitten part followed by dry gangrene. Early shock is common and is the main cause of death. Bleeding may be delayed for up to several days. The blood clots poorly because of absent or very little fibrinogen.

Monitor bleeding time, coagulation time, prothrombin time and platelet count at least 4 hourly. Investigation - Full blood count - Hb, platelets count - Urine for haemoglobinuria or myoglobinuria - Coagulation screen — BT, CT, PT, PTT - Serum electrolytes, particularly the potassium levels - ECG Snake Venom - Snake venom varies greatly, from species to species and among the different varieties of the same species and also even from time to time from the same snake.

Proteins contribute more than 90 percent of the dry weight includes enzymes, peptides, glycoproteins and other substances. The limb is then immobilized with a splint. Minimize movement of the limb. Keep the limb below the level of the heart. Please do not attempt to kill the snake, as this may be very dangerous.

Use the snake bite chart Table Fasciotomy may be required if there are signs of compartment syndrome. Local necrosis and gangrene may require orthopedic or vascular surgical consultation for debridement. Grade Dosage Grade 1: Minimal There is minimal envenomation, and snakebite is suspected. A fang wound is usually present.

Pain is moderate or throbbing and localized to the fang wound, surrounded by 1 to 5 inches of edema and erythema Not indicated Grade 2: Moderate More severe and widely distributed pain, edema spreading toward the trunk, and petechiae and ecchymoses limited to the area of edema.

Nausea, vomiting, giddiness, and a mild elevation in temperature 2 - 4 vials Grade 3: Severe Petechiae and ecchymoses may be generalized. Systemic manifestations may include tachycardia, hypotension, and a subnormal temperature.

Laboratory abnormalities includes elevated white cells count leucocytosis , coagulopathy abnormal aPTT, PT, fibrinogen degradation products, thrombocytopenia, increased bleeding time , deranged renal and liver function. Very severe Sudden pain, rapidly progressive swelling that may reach and involve the trunk within a few hours, ecchymoses, bleb formation, and necrosis.

Systemic manifestations, often commencing within 15 minutes of the bite, usually include weakness, nausea, vomiting, vertigo, and numbness or tingling of the lips or face, muscle fasciculations, painful cramps, pallor, cold clammy skin.

Present -: Absent Speech N: Normal S: Slurred Tongue Protrusion N: Normal W: Weak Breathing N: Liberal use of antibiotics for prophylaxis in snake bite is not required. However bites by certain species especially Malayan pit viper are likely to be complicated by bacterial infections as the venom or fangs are often contaminated with microorganism.

In this case prophylaxis antibiotic may be indicated. Antivenom - Antivenom is the cornerstone of treatment of venomous snake bites. Snake bites are usually defensive acts, hence the dose of venom injected is usually small. As such, there is a risk of anaphylaxis. Patients with atopy are especially vulnerable. The intravenous route is the most effective. Antivenom therapy is indicated if the victim develops one or more of the following systemic symptoms and also based on the grade of envenomation see Table To be specific, antivenom must be specific to the species of the snake responsible for the bite, therefore monovalent antivenom is ideal if the the biting species is known, however polyvalent is more popular as in majority of cases the snakes cannot be identified.

The doses of anti-venom depend on the make and type. The effective dose also depends on the potency of the anti-venom. Inadequate anti-venom can result in envenomation persisting.

The dose for children is the same as adult. There is NO maximum dose of antivenom. Reconstitute antivenom can be given either slow intravenous push or diluted in isotonic fluid and administered over 1 hour. Reconstituted antivenom should be used immediately. If there are no reactions, the antivenom is infused over 30 minutes to 1 hour. The infusion should be administered under close monitoring of cardiac function and vital signs. Adrenaline, hydrocortisone and antihistamine solutions must be at hand for treatment of anaphylaxis.

Antivenom is produced either liquid form or freeze dried. Liquid antivenom is very unstable at room temperature and must be stored in a dark, cool place with temperature degree Celcius. Anti-venoms have a limited shelf life and its potency may decrease with time.

Symptoms include itching, urticaria, cough, nausea, vomiting, fever and palpitations. A small percentage may develop severe anaphylactic shock which characterized by hypotension, bronchospasm and angioedema. Symptoms include fever, rigor and vasodilatation with febrile convulsion can occur in children. Clinical features includes urticuria, fever, athralgia, periartucular swellings occur, lymphdenopathy and proteinuria. Patient can be started on a 5 days course of antihistamine and in severe cases or those fail to respond in 24 to 48 hours, oral prednisolone for 5 to 7 days is indicated.

C adrenaline 0. Should any features of allergy appear, stop the infusion and institute further treatment with adrenaline. Give the anti- venom in small and divided doses under careful observation.

Mechanical ventilation should be initiated followed by intensive care support.


All the effect of neurotoxins is eventually reversible. Adequate amount of volume replacement which includes crystalloids, colloids and blood may be required to correct the volume deficit. Do not disturb the blisters, it will heal completely if no underlying necrosis. Local swelling usually will resolve after adequate dose of antivenom. Increased intra compartmental pressure within the tight fascial compartment due to tissue oedema leading to ischaemia and subsequently necrosis.

The main signs include severe pain, swelling, muscle weakness and hypoeasthesia. Fasciotomy should be done after correction of blood coagulation.

This complication can be avoided if antivenom is given early. Bigatelo LM et al Ed. Renal Failure in Cirrhosis. N Engl J Med; Bosch X et al Rhabdomyolysis and Acute Kidney Injury. Acute renal failure: Crit Care 8: Defining acute renal failure: Physiological principles.

Intensive Care Med Developing a classification system for acute renal failure. Curr Opin Crit Care 8: Bellomo R et al Adv Ren Replace Ther, Oct;9 4: Chapter 10 Poisoning 1.

Clinical Policy: Critical issues in the management of adult patients presenting to the Emergency Department with acute Carbon Monoxide poisoning. Shirley Ooi, Peter Manning. Guide to the Essentials in Emergency Medicine. McGraw Hill — Education. Concept and Clinical Practice. Elsevier Health Sciences.

A Vale, N Bateman. N Bateman. The epidemiology of poisoning. A Vale and S Bradberry. Assessment and diagnosis of poisoned patient. Drugs and toxins that damage the kidney. Advances, challenges and controversies in poisoning.

Emerg Med J. A Parfitt, JA Henry. Troublesme toxins. Critical issues in management of patients presenting to the Emergency Department with Acetaminophen overdose. Ann Emerg Med. Diagnostic criteria and early management of pesticide poisoning. Clinical procedures in emergency medicine 4 th Ed.

Saunders Publications. Adult Toxicology in Critical Care: Part 1: Multiple dose activated charcoal in acute self poisoning: Chapter 11 Poisonous Snake Bites 1. Malaysian Immunisation Manual 2 nd Edition.

College of Pediatric and Academy of Medicine, Malaysia 3. Terry and K. Best evidence topic report. The use of antibiotics in venomous snake bite. Emergency Medicine Journal. Subang Jaya. Contributors Dr. Malaysia Dr. Malaysia Senior Lecturer. I am so happy that two decades later.

It was sold at RM5. I found that there were some sections which needed very little revision. Johor Bahru Clinical School. In updating the book for this edition. When he approached me to ask for permission to create a completely revised version in which specialists in their own field will each review and contribute a chapter. I have contacted Dr Wong for his permission to update this book and published it as an ebook.

I was gratefully happy. This ebook is not meant to compete with other much better emergency medicine guides. Med Emerg Med. I have added entirely new chapters. In certain instances.

I found my old copy two years ago and felt that it is a waste to let it go. MB ChB Manchester. Malaysia October Acknowledgement This book would not have been possible without the generous support of many people. This ebook will not be restricted to Internal Medicine specialities but may include topics from other areas of medicine such as psychiatry.

Dr Tan Swee Looi — for script reading. This ebook has many appeals. Description The first edition of the Guide to the Essentials in Emergency Medicine, co-edited by two prominent emergency physicians, Associate Professors Shirley Ooi and Peter Manning, with a combined total of 64 years of Emergency Medicine practice between them, was first published in Singapore in This book focuses on the practical management of the most life-threatening and common conditions encountered by emergency physicians.

It is designed to offer a balanced viewpoint advocating the tenets of evidence-based medicine. This second edition preserves several of its predecessor's hallmark features. Easy-to-read format: Popular sections such as Caveats, covering the pitfalls likely to be encountered in medical practice, and Special Tips for GPs are retained. New features of this second edition include: Product details Format Paperback pages Dimensions Includes tips for GPs like me. Paperback2nd editionpages.

Do you shirley ooi emergency medicine other people are making progress much faster than you? Rewire your belief system. Are you getting left behind? Shopbop Designer Fashion Brands.

She has received multiple research grants and published multiple articles in peer-reviewed journals. Dewa P rated it liked it Dec 30, Goodreads helps you keep track of books you want to read. Thanks for shirley ooi emergency medicine us about the problem. She is also a reviewer with the Annals of the Academy of Medicine of Singapore.

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