Based on the very good medical book of Stone C.K., Humphries R.L., Current Diagnosis and Treatment in Emergency Medicine, McGraw Hill - LANGE, 6th edition, 2008. mcgraw-hillmedical.com 
and

the very good manual book of Longmore M., Wilkinson I., Turmezei T., Kay Cheung C., Oxford Handbook of Clinical Medicine, Oxford Medical Publications, 7th edition, 2008. www.oup.com

NOTE

All the medical procedures and drug administration mentioned in this text should be done only under a senior doctor’s consultance.

(A)   GENERAL ADVICES IN AVOIDING PITFALLS IN EMERGENCY & ACUTE MEDICINE (FOLLOWED ONLY AFTER A SENIOR DOCTOR’S CONSULTANCE)

·        Administration of medications (such as adrenaline) on peripheral lines on emergencies should be followed immediately by flush with normal saline (at least 20 ml for adults and 2 – 5 ml on children) and elevation of the extremity for 10 – 20 sec to facilitate drug delivery to the central circulation. 

·        Avoid saline on patients with decompensated liver failure (e.g. ascites, oedema) because it worsens ascites (patients have high body sodium despite the low serum sodium). Use instead salt poor albumin or whole blood for resuscitation and 5% dextrose for maintenance. 

·        In severe hypothermia with cardiovascular instability one way of rapid core rewarming is thoracic cavity lavage with 2 thoracostomy tubes and infusion of fluids warmed to 41 C⁰ (105.8 F⁰ ) thru one tube and drainage thru the other one. However in case of non severe and without cardiovascular instability hypothermia, rapid rewarming is hazardous! So, on not severe hypothermia, especially on elderly, do slow rewarming (increase temperature by 0.5⁰ C / hour). Otherwise you may induce hypotension! On immersion with severe hypothermia, rapid rewarming is needed. In case you use bypass, don’t give heparin if trauma.

·        Gamma – Hydroxybutyrate is a CNS depressant and can cause coma. It is called ‘date rape drug’ and it is used often on rave parties. Treatment is supportive and includes endotracheal intubation if airway is compromised.

·        PCP (phencyclidine) poisoning has rapid onset of action (smoked or snorted), symptoms may fluctuate from severe agitation and paranoid/violent behaviour to stupor and may also include vertical and horizontal nystagmus, hyperthermia and rabdomyolysis with myoglobinuria (which may cause ARF – acute renal failure). Pupils are small or large. Also may have hypertension and tachycardia. The drug is manufactured from marijuana, amphetamines and hallucinogens. So it is sympathomimetic and hallucinogenic. Treatment is supportive with GI (gastrointestinal) decontamination, diazepam for agitation, and in case of rhabdomyolysis, hydration with IV fluids, mannitol for urination and alkalization of urine. 

·        Basilar artery occlusion can be manifested as coma, altered mental status, irregular respirations, papillary abnormalities (poor reactive pupils of normal size 3mm or fixed in mid position 5 mm pupils or pinpoint pupils), conjugate eye deviation away from the side of lesion, absent or abnormal horizontal movements during calorics or doll’s manoeuvre (vertical eye movements may be intact), positive Babinski (upgoing plantars – with dorsiflexion), increased reflexes and hemiparesis. The patient may have history of TIAs (transient ischemic attacks) of basilar artery that are manifested with dizziness, diplopia, ataxia, weakness, N&V (nausea & vomiting) and slurred speech.

·        Basilar artery insufficiency may have similar with the above symptoms. It is caused usually from atherosclerosis. Symptoms are often positional (!) and may occur with e.g. neck extension or rotation at a particular side. Most common symptoms are vertigo, visual problems (such as diplopia), episodic perioral numbness or paresthesias, dysarthria, ataxia, syncope, headache, nausea, vomiting, tinnitus and cranial nerve dysfunctions. So basilar artery insufficiency may be confused diagnostically with vestibular problems (especially benign positional vertigo), headache, syncope, cerebellum problems, posterior columns problems & loss of proprioception, subclavian steal syndrome.

·        Subclavian steal syndrome is caused by stenosis of the subclavian artery proximal to the vertebral artery root. Symptoms may include vertigo and syncope with left arm exertion (!), angina and ulcerated or gangrenous hands! BP and pulses of the upper extremities are usually unequal! Usually there is a 45 mmHg decrease in systolic BP in the arm supplied by the stenotic artery.

·        On unclear cause of shock, exclude hypovolaemia and especially ruptured abdominal artery aneurysm.

·        Anaphylactoid reaction results from direct release of mediators from inflammatory cells, without antibody release, usually from drugs such as N – acetylcysteine (antidote for paracetamol/ acetaminophen poisoning).

·        Pulmonary oedema may be caused by LVF (left ventricular failure), mitral stenosis, arrhythmias, malignant hypertension, ARDS, trauma, infection (e.g. malaria), post operative, drugs, sepsis, drug overdose, illicit drug abuse, fluid overload, renal failure, neurogenic (e.g. head trauma). The most common cause is cardiogenic.

·        Differential diagnosis of acute breathlessness includes pulmonary oedema/ heart failure, (tension) pneumothorax, asthma/ COPD, pneumonia, PE pulmonary embolism (here we may have hemoptysis), metabolic acidosis (e.g. DKA diabetic ketoacidosis), drug poisoning (e.g. salicylates), anaphylaxis (wheezing/ stridor), foreign body airway obstruction (child, mental ill, stroke), pneumonia etc.

·        Differential diagnosis from pulmonary oedema, asthma/COPD and pneumonia may be difficult. These may co-exist, especially on the elderly, and may be hard to distinguish. However wheeze in pulmonary oedema is considered as ‘cardiac asthma’. Other signs of pulmonary oedema are pulsus alterans (alternation strong and weak pulse that shows LVF left ventricular failure), increased JVP jugular vein pressure (check for JVD jugular vein distension), fine lung crackles (inspiratory, especially at the bases, in doubt ask the patient to cough and check if the crackles continue), gallop rhythm (S1S2S3), orthopnea, tachycardia, tachypnea, shortness of breath and may have pink frothy sputum.  If unsure for diagnosis, plasma BNP (brain natriuretic peptide) may help to ascertain the diagnosis. Check CXR (chest X’ Ray) for cardiomegaly, Kerley B lines, butterfly/ butt picture. With ECG and Troponins exclude MI (heart attack) and consider cardiac Echo. rh (recombinant) BNP (Nesiritide) may be useful in heart failure short term treatment, but is used only in decompensate cardiac failure.

·        Tension pneumothorax is manifested with breathlessness, tachycardia, hypotension, pleuritic chest pain, hypoxia, increased percussion (hyperresonance) & decreased breath sounds on the affected side. Also is manifested with tracheal deviation away from the affected side and, if not hypovolaemic, JVD jugular vein distension. 

·        Causes of tension pneumothorax.  Tension pneumothorax may occur spontaneously (especially on tall young thin males), or due to rupture of a subpleural bulla. Other causes are asthma, COPD, TB, lung abscess, pneumonia, sarcoidosis, lung cancer, CF cystic fibrosis, lung fibrosis, Marfan’s, Ehlers Danlos and trauma. It may also be iatrogenic (the most common cause) such as after subclavian CVP line insertion, pleural aspiration or biopsy, positive pressure ventilation and liver biopsy.  Treatment is with immediate decompression (don’t wait for CXR Chest X’ Ray!).

·        If heart failure does not respond to therapy, then consider other diagnosis such as aortic dissection, hypertensive crisis, pneumonia, pulmonary embolus and asthma/COPD.

·        On COPD patients start oxygen at 24 – 28%. Check ABGs (arterial blood gases). Some patients rely on their hypoxic drive to breathe, so oxygen more than 30% may lead to reduced RR (respiratory rate) and hypercapnia which will cause decreased conscious level and respiratory failure with cardiac arrhythmias. So, in case on ABGs is evidence of CO2 retention, start with 24 – 28% oxygen in the above patients and reassess after 30 min. In case the patient has not evidence of CO2 retention then start with 28 – 40% oxygen and monitor next the ABGs.

·        Therapy of COPD is with oxygen (see above), bronchodilators (salbutamol + ipratropium) and IV hydrocortisone (or PO prednisolone). If you suspect infection give e.g. amoxicillin. If no response, consider adding aminophylline (don’t give loading dose if the patient is already on methylxanthines). If still no response, consider NIPPV ventilation, or intubation & ventilation (especially if acidosis and hypercapnia).

·        CURB – 65 are the core adverse features of pneumonia and include Confusion (e.g. abbreviated mental examination test <_8), Urea> 7 mmol/L, RR (respiratory rate) >_30/min, BP< 90/60 mmHg and age >_65. Score 0 – 1 means that home treatment is possible. Score 2 necessitates hospital treatment. Score >_3 indicates severe pneumonia – consider ICU.

·        Risk factors for PE (pulmonary embolism are) malignancy, surgery (especially hip/ pelvis), prolonged immobility, oestrogens (contraception – the Pill & HRT hormone replacement therapy), thrombophilia and history of TE (thromboembolism).  PE manifests usually 10 days after a major surgery (especially on hip or pelvis) and especially after straining at stool!

·        In case of massive pulmonary embolism don’t give heparin if you suspect septic embolism (e.g. right sided endocarditis). 

·        PE (pulmonary embolism) symptoms may include respiratory distress, increased respiratory rate, tachycardia, pleuritic pain (on inspiration) and hemoptysis. Massive pulmonary embolism may manifest with cardiac arrest. Main stem of therapy is 100% oxygen and heparin IV. Consider also thrombolytics or surgical embolectomy in massive PE.  In case of hypotension give colloids IV and inotropes (remember that noradrenalin needs always a central IV line).

·        PE pulmonary embolism (investigation): Check D’ Dimmers, ECG (may have just sinus tachycardia, may have deep S in I, Q waves in III and inverted T waves in lead III: SI QIII TIII – but it is rare; may also have right axis deviation, may have right ventricular strain – T inversion on V1 – V3), CXR (Chest X’ Ray, changes are not specific), CBC (FBC Full Blood Count), ABGs (Arterial Blood Gases: decreased PO2, PCO2, PH, bicarbonate, also metabolic acidosis, but PH may be increased), coagulation studies, Doppler of legs and pelvis, Spiral CT or V/Q lung scan. The gold standard test is pulmonary angiography.  Normal D’ Dimmers exclude tromboembolism. If D’ Dimmers are increased, perform a spiral CT or a V/Q lung scan.

·        The risk for thromboembolism (TE) is big during whole pregnancy and puerperum. (75% of thromboembilisms occur before the labour, but pulmonary embolism happens more often after the delivery), history of TE (personal or family history), severe obesity, immobility, long trips (>3 hours), varicose veins, thrombophilia (V Leiden mutation, protein C or S deficiency,  lupus anticoagulant, homocysteinaemia, antithrombin III deficiency, cardiolipin antibody, G20210A mutation of the prothrombin gene and dysfibrinogenaemia).  

·        Prevention of TEs (thromboembolisms) is with LMWH (low molecular weight heparin) Sc, compressive stocking and good hydration (especially in summer and during long trips - in the last case the patient may take prophylaxis with aspirin).

·        In case the patient has pain on the calf exclude DVT (deep vein thrombosis). The calf may be warm, with oedema, tender, red, and the patient may have increase in temperature. Perform leg & pelvis to check the iliacofemoral veins) Doppler and plythismography and check D’ Dimmers. The gold standard test is venography. WBCs may be increased. Avoid Homan’s manoeuvre (passive dorsal flexion of the foot) because it may detach the clot! The left calf is affected more frequently on pregnant. A deference of > 2 cm perimeter on measuring the legs with a measure tape indicates DVT. The patient may have DVT deep vein thrombosis also on her pelvis veins, so perform a leg Doppler as well as a pelvis Doppler (to check the iliacofemoral veins) in case you suspect DVT/ TE/ PE.

·        The causes of upper GI (gastrointestinal) bleeding are 40% PUD (peptic ulcer disease), 15% Mallory Weiss tear (after retching!), 10% gastroduodenal erosions, 10% oesophagitis, 7% oesophagal varices and the rest cases are from cancer, AV malformations and haemoptysis from swallowed blood. 

·        On GI bleeding, perform (with a NG nasogastric tube) gastric lavage (with room temperature normal saline) and check if there is blood on aspiration. If there is, then the bleeding is proximal to Treitz ligament. If there isn’t, then the bleeding is distal to the Treitz ligament. In the last case, exclude duodenal ulcer (if not bile on gastric aspiration, also 10% of gastric aspiration is negative) or aorto-enteric fistula (history of aortic aneurysm surgery). On GI bleeding exclude Osler – Weber – Rendu syndrome (hereditary haemorrhagic telangiectasia, telangiectasia e.g. lips, face, fingers, history of GI bleeding and/or epistaxis), Mallory Weiss tear (after severe retching or vomiting) and mesenteric ischemia (severe abdominal pain with bloody diarrhoea or melena)!

There are also many other reasons of GI bleeding to exclude on differential diagnosis. Test also faeces for occult blood and also put a Foley urinary catheter. Blood in urine may indicate an abdominal aneurysm! On positive NG tube lavage or negative lavage with active lower GI bleeding (on continuing bleeding, and unstable patient) call a gastroenterologist (for emergency endoscopy on upper GI bleeding and colonoscopy on lower GI bleeding) and a general surgeon. On upper GI bleeding from oesophagal varices or PUD (peptic ulcer disease) consider giving octreotide (and omeprazole on PUD and gastritis). History of oesophageal varices does not mean that the upper GI bleeding is from them but may be from another source (e.g. gastric). On lower GI bleeding exclude gastroenteritis (e.g. with Shigella) or pseudomembranodous colitis (from Clostridium difficile after antibiotics) and IBD (inflammatory bowel disease). 

On lower GI bleeding consider mesenteric angiography or scintigraphy (with labelled RBC with 99m Tc). On upper GI bleeding consider ET (endotracheal) intubation on altered mental status and/or profuse hematemesis. 

·        On anaphylaxis don’t forget to raise the feet and give adrenaline IM (0.5 mL 1: 1000), 100% oxygen, IV fluids (0.9 saline e.g. 500mL over half an hour – you may need up to 2 L), chlorphenamine (10mg IV), hydrocortisone (200 mg IV), salbutamol (if wheeze) and inotropes on persistent hypotension. Also consider early intubation (RSI). If the intubation is difficult because of the neck oedema, call a senior anaesthetist and a surgeon for tracheotomy. If ET (endotracheal) intubation and BMV (bag mask ventilation) aren’t effective and there is not enough time (and the anaesthetist or the surgeon haven’t arrive), and the laryngeal oedema is life threatening, perform PTTJV (percutaneous transtracheal jet ventilation) or perform cricothyroidotomy (e.g. with a ‘mini Trach’ set). PTTJV is useful on a child (also useful in epiglotitis and foreign body obstruction above the cricoid level), where tracheotomy needs an expert ENT or an experienced surgeon.

·        Exclude anaphylaxis if wheezing, urticaria/ rash/ erythema/ itching, angio/oedema (larynx, lids, lips, tongue, uvula), laryngeal obstruction – stridor (exclude foreign body obstruction e.g. child, mental ill, stroke), cyanosis, hypotension/ shock and tachycardia.  Give immediately adrenaline IM 0.3 – 0.5 mg (0.3 – 0.5 mL 1:1000) on adults or 0.01 mg/kg on children.

·        Contraindications to LP (lumbar puncture) are suspected intracranial mass lesion, papilloedema, focal neurological signs, trauma, middle ear pathology, major coagulopathy and septemic signs of meningitis with shock, hypotension, rash (initially may have decreased capillary refill >2sec and cold hands & feet). Be aware of the above contraindications, because if you perform a LP the patient may die from herniation!

·        Suspect encephalitis if odd behaviour, decreased level of consciousness, cranial nerve lesions or palsies/ paralysis. Often there is a prodrome with fever, lymphadenopathy, rash, conjuctivitis, meningeal signs, and seizures). Causes are EBV, CMV, HSV, toxoplasmosis, measles, arboviruses and Japanese B or West Nile encephalitis. In HSV (herpes simplex virus) encephalitis give IV acyclovir. Tests are blood & throat/ CSF, urine viral culture/PCR/ virology tests/ antibodies, enhanced CT, toxoplasma antibodies. Dexamethazone IV is also used. 

·        Pseudoseizures (fake seizures) if odd features such as pelvic thrusts, arms and legs flailing around and also on resisting attempts to open lids and to do passive movements. Research has demonstrated that a great proportion of seizures are in fact pseudoseizures!

·        Lorazepam on seizures (4mg) must given slowly (<_ 2min) into a large vein, because fast administration may induce respiratory arrest!

·        Cerebral abscess has to be suspected if the patient has increased ICP (intracranial pressure), fever, or increased WCC. Signs are seizures, fever, signs of increased ICP or localizing signs, coma and signs of sepsis elsewhere (e.g. teeth, ears, endocarditis, lungs/ bronchiectasis, sinuses) or skull fracture or congenital heart disease. Perform CT/MRI.

·        Pheochromocytoma may manifest with hypertensive crisis (pallor, pulsating headache, hypertension, doom feeling), and may be produced by stress, parturition (labour), general anaesthetics, contrast media in radiology and abdominal palpation. Treatment is with phentolamine 2 – 5 mg IV (repeat to maintain BP). Alternatively use labetalol. When BP is controlled give phenoxybenzamine and a β1 blocker for tachycardia.

(B) EMPIRICAL ADVICES IN AVOIDING PITFALLS IN EMERGENCY & ACUTE MEDICINE (FOLLOWED ONLY AFTER A SENIOR DOCTOR’S CONSULTANCE)

·        Always in all your patients perform ABCDEs consider the 4Hs & 4Ts and also ask AMPLE, regardless the patient’s condition (e.g. a minor trauma or a patient that appears well). For example a patient arrives in the ER (A&E) and reports that he had a fight with his friend. He looks well. Suddenly he suffers respiratory distress and his BP is falling and he is hemodynamically deteriorating.

On exposure you see a lateral chest stab and suspect tension pneumothorax which you treat. After the patient is stabilized you ask him why he didn’t report the stab and he replies that his boy friend stabbed him when he learned that he was HIV positive!

In this example you could lose the diagnosis and perhaps making another wrong diagnosis (such as severe arrhythmia).

But performing ABCDEs you should see on A tracheal deviation and on B you will notice increased respiration rate, ipsilateral decreased breath sound and hyperesonant percussion.  On C you will notice tachycardia, hypotension, normal (and not muffled) S1, S2, no pulsus paradoxus, no Kussmaul sign (excluding cardiac tamponade), tachycardia on cardiac monitoring (without electrical alterans). You will also notice distained neck veins.

On E (exposure) you will see the stab on the chest.  Considering these clues you make the possible diagnosis of tension pneumothorax which by the way decompress with a needle (and next a thoracostomy tube) and you don’t wait for CXR (chest X’ Ray).

I remind that A is Airway (including neck immobilization), B is Breathing, C is Circulation, D is Disability (AVPU, or better, GCS, also pupils’ size, reaction to light, equality and body posture) and E is Exposure and also prevention of hypothermia and Expert call!

·        Patient’s Exposure is very important and don’t avoid it because you or the patient feel embarrassed. It may give you diagnostic clues such a trauma on the back or a rash that indicates allergy (e.g. urticaria) or meningitis (e.g. 1 or 2 or more petechia that don’t blanch on glass).

·        Meningitis may appear without meningitic signs (e.g. neck stiffness and photophobia), but with septemic signs of shock (cold hands, decreased capillary refill > 2sec, later hypotension) and rash. In the last case (of septemic signs) don’t do LP (lumbar puncture), but give antibiotic (e.g. cefotaxime 2 – 4 gr slowly IV every 8 hours) and transfer to ICU!

·        On chest pain don’t forget to palpate the abdomen (e.g. exclude duodenal ulcer perforation). Also on epigastric pain don’t forget to do an ECG (MI) and a CXR (Chest X’ Ray e.g. pneumonia of the bases).

·        By asking always AMPLE (Allergy Medication Past medical history Last Meal and Environment of the event) you may have many diagnostic clues.

·        On orthopaedic problems exclude gonorrhoea (arthritis, may have rash), TB, Brucellosis, gout and pseudogout (crustal arthritis). But first with joint aspiration, analysis, microscopy, stain and culture exclude septic arthritis and osteomyelitis. Consider, also, rheumatologic diseases, especially RA. For further evaluation consider X’ Rays, CT/MRI, Bone Scan and arthroscopy.  

·        Always consider allergy/ anaphylaxis on your differential diagnosis. For example a patient appears on the ER and says that accidentally he spoiled with paint his face and body. He looks well, however suddenly deteriorates. He is short of breath and has stridor. A stridor has to alarm for an allergy (or angioedema) or airway obstruction by a foreign body (especially on a child or a mentally incapacitated or a psychiatric patient or a patient with a stroke). So the above patient had allergy to the paint and not immediately reacted with anaphylaxis. Anaphylaxis is a diagnosis that must not be missed. A single IM adrenaline shot may be life saving.

·        Asking AMPLE and taking a brief history (from the patient, the relatives, the paramedics, the patient’s GP and perhaps neighbours or the police) is essential. For example a patient may appear with hematemesis. He doesn’t mention any peptic ulcer disease (PUD), however he mentions that he had a fight with 2 guys 2 days ago and they punched him on his abdomen. You suggest that the GI (gastrointestinal) bleeding has traumatic origin. However, after a thorough history approach, the patient admits that he had abdominal pain after the assault and took many (he can’t remember how many) OTC painkillers (without remembering what has the drugs name). You suppose he took NSAIDs.

The toxicology screening (for aspirin and acetaminophen) shows that he took acetaminophen (paracetamol) that caused the bleeding disorders after causing severe acute liver failure. Although the patient came in hospital later than 15 hours from paracetamol ingestion, you still consider of giving N acetylcysteine IV as antidote (you have nothing to lose). The patient’s INR is 3, so with INR >2 on <48h or >3.5 at <72h you consider transferring the patient to a specialist liver unit. Other later complications from paracetamol poisoning are encephalopathy (from liver failure) and renal failure (check if creatinine is > 200 μmol/L).  

Don’t forget that N – acetylcysteine may cause an anaphylactoid reaction! It manifests with wheezing, shock and vomiting and occurs on less than 10 % of the patients. In that case stop the drug. However don’t stop the antidote infusion if the patient develops a rash. In that case give chlorphenamine (an antihistamine) and observe if an anaphylatoid reaction develops.

·        The above patient with liver insufficiency had as result upper GI (gastrointestinal) bleeding. In this case (and also if a patient is taking warfarin) consider giving vitamin K and FFP (Fresh Frozen Plasma). 

·        Always ask AMPLE and always do ABCDEs and don’t forget E –Exposure (and Expert call). For example a junior nurse with allergy on Latex, that she is unaware of, appears with sudden respiratory distress and cardiovascular instability. You ask AMPLE, but she doesn’t report any allergy. However, on her skin she has urticaria that you may miss if you don’t expose the patient! Other signs of anaphylaxis are itching, angioedema, erythema, oedema, cyanosis, wheezing, laryngeal obstruction with stridor and hypotension. An atopy history may or may not be suggestive (not all that have atopy develop anaphylaxis).

·        Also always on a deteriorating patient or a patient on arrest consider the 4 Hs and 4 Ts whish are hypoxia, hypovolaemia, hepo/hyperkalaemia/metabolic problems and Hypothermia. The 4 Ts are Tension pneumothorax, Tamponade cardiac, Toxins (poisoning/drugs/ medication) and Thrombosis (cardiac or pulmonary). The 4 Hs and 4 Ts are reversible causes of sudden deterioration and cardiac arrest.

·        Symptoms occurring on more than one persons, or on a family may indicate poisoning.

·        If the patient manifests with neurological symptoms exclude poisoning (e.g. parathion, organophosphates, carbamate, Lead, Arsenic, CO carbon monoxide etc.), botulism (eating home tins, babies eating honey) and shell fish toxins. Check the electrolytes (exclude hyper/hypokalaemic periodic paralysis), do toxicology screening and call the poisoning center. Also consider tick paralysis (remove the tick) and Lyme disease. To exclude brain problems perform initially a non contrast CT. Also perform LP (lumbar puncture) to exclude meningitis, meningoencephalitis, subarachnoid haemorrhage. However, be causious on LP contraindications.  On subarachnoid haemorrhage it may take 2 – 4 hours for CSF xanthochromia after the bleeding! Increased bilirubin – jaundice, elevated CSF protein and hypercarotonemia  may also cause xanthochromia! Don’t forget to take a CSF specimen for a VDRL study.  Also measure opening pressure!

·        In case you suspect poisoning, but you haven’t any clues, ask the family, paramedics, friends or neighbours. If still no clues, ask the police to go at the place (e.g. home) in which the victim was found.

·        On poisoning don’t forget decontamination, skin and eyes cleaning, clothes removal, gastric lavage, activated charcoal and/or whole bowel irrigation. Also think antidotes! 

·        On neurological problems do not forget fundoscopy (however do not instal mydriatic eye drops before the neurological examination and GCS is completed). Retinal vein pulsation at fundoscopy may exclude increased ICP (intracranial pressure), however it is absent in 50% of normal population! But absence of venous pulsation at the disc is a useful sign. On the other hand, papilloedema isn’t always a reliable sign.

·        A pregnant woman may appear with a sudden problem that is irrelevant to pregnancy (however, off course, you will need to exclude the obstetric emergencies such as placenta abruption, ectopic pregnancy and uterus tear – ask if previous C section! Also check BP and urine protein to exclude eclampsia). For example a pregnant woman is brought to the ER with loss of consciousness and hypoternsion. You ask the paramedics about the history and they refer that one of her friends mentioned that the pregnant said her that she visited on the morning an ENT doctor that diagnosed otitis media. You suspect otitis media complications. You perform a LP (lumbar puncture) which is positive for meningitis! Note: many books mention that LP is contraindicated in septicaemic signs of meningitis (cold hands and feet, rash, increased capillary refill time > 2 sec, later hypotension) and also on middle ear pathology, so in this case LP was contraindicated! You take antibiotic prophylaxis yourself (ciprofloxacin or rifambicine. The only problem is that the antibiotics may be dangerous for the foetus. You consult an obstetrician who recommends C section and delivery of the baby. If the LP was clear, then other complications of the otitis media (such as brain abscess or cavernous sinus thrombosis) could be excluded with a head CT.  On the above case, perhaps the antibiotics should be given as soon as possible, after consulting BNF/ FDA for the toxicity to pregnant.

·        A vasovagal syncope may occur from cough, micturition, defecation, migraine, pain, prolonged standing, sudden exposure to cold, sight of blood, loss of blood and on a surgical/ interventional procedure. It can also occur by drinking cold water! This kind of syncope can be reproduced on the ER. It is characterised by sudden bradycardia after vagal stimulation. Therapy is by avoidance of the specific stimuli!  

·        Poisoning from the plant tobacco gigante may cause nicotine poisoning. Nicotine poisoning, as well as poisoning from aconitine, (from plants) cause vomiting, salivation, diarrhea, restlessness and seizures. They also may cause mydriasis. Initially they cause excitement. Severe poisoning may cause hypotension and respiratory depression. Active charcoal may be beneficial in some cases.

·        In case of cardiac trauma with tamponade, if you perform open surgery, then during the wound suture be careful not to put a stitch the coronary artery or its branches. In that case, the monitor will show myocardial ischemia!

·        Overdose may occur with pills that are used unlicensed (often tracked on the internet) for losing weight or for body building. These pills may contain caffeine, ephedra, ephedrine, thyroxin, anabolic steroids and other dangerous substances. Poisoning may cause severe arrhythmia.

·        A bullet or a sharp object may enter very rarely thru the eye pupil or the external meatus of the ear or the nasal meatus and enter the brain without any sign of external trauma. The object will appear on an X’ Ray or a CT! 

·        Collapsus after straining at stool may occur due to cerebral haemorrhage or pulmonary embolism or vasovagal syncope.

·        Protamine sulphate is antidote for heparin overdose. Vitamin K & FFP (fresh frosen plasma) are antidotes for warfarin overdose.

·        Asterixis with reactive pupils may indicate metabolic encephalopathy. Check biochemistry and electrolytes. Also check thiamine and vit B12.

·        Unequal upper extremity pulses and systolic BP may indicate subclavian steal syndrome, aortic dissection, aortic rupture (if trauma), or aortic arc aneurysm rupture!

·        On patients with fixed cardiac output  (e.g. HOCM hypertrophic obstructive cardiomyopathy or aortic stenosis or mitral stenosis) avoid drugs that may lower BP (such as nitrates or ACE inhibitors).

·        When starting an ACE inhibitor withdraw diuretics 24 – 48 hours before, otherwise severe hypotension may occur. They can be restarted once treatment has been initiated (usually in lower dose). Give initially a small dose of ACE inhibitor (e.g. 6.25 mg captopril or 2.5 mg enalapril) only when the patient is on bed, because the initial dose may cause, within 4 hours of the administration, a transient severe fall in BP.

·        Verapamil is a negative inotropic agent so avoid it in patients with left ventricular impairment or heart failure, even they are stable! Also, avoid it on 2^nd or 3^rd degree heart block, sick sinus syndrome. Don’t give concomitantly a Calcium channel blocker with a β’ blocker, because they may cause severe hypotension and bradycardia.  

NOTE

All the medical procedures and drug administration mentioned in this text should be done only under a senior doctor's consultancy. Some information in this text is empirical and its reliability can't be ascertained. It is suggested to search official medical articles, books and guidelines in order to ascertain the medical information of this text.

NOTE

About PE (pulmonary embolism), negative D - Dimers are helpful and may rule out only low risk patients. On high risk patients perform a spiral CT or V/Q scan.

BIBLIOGRAPHY FOR EMERGENCY & ACUTE MEDICINE

1)Stone C.K., Humphries R.L., Current Diagnosis and Treatment in Emergency Medicine, McGraw Hill - LANGE, 6th edition, 2008.

2)Wyatt J.P., Illingworth R.N., Graham C.A., Clancy M.J., Robertson C.E., Oxford Handbook of Emergency Medicine, Oxford Medical Publications, 3rd edition, 2006.

3)Ramrakha P., Moore K., Oxford Handbook of Acute Medicine, Oxford Medical Publications, 2nd edition, published 2004, reprinted 2005.

4)ALS (Advanced Life Support), European Resuscitation Council, 5th edition, The Image Factory, Belgium,2006.

5)EPLS (European Paediatric Life Support), European Resuscitation Council, 3rd edition, The Image Factory, Belgium, 2006.

6)Llewelyn H., Aun Ang H., Lewis K., Al – Abdulla A., Oxford Handbook of Clinical Diagnosis, Oxford Medical Publications, 2006.

7)Thomas J., Monaghan T., Oxford Handbook of Clinical Examination and Practical Skills, Oxford Medical Publications, 2008.

8)Richards D., Aronson J., Oxford Handbook of Practical Drug Therapy, Oxford Medical Publications, 2008.

9)ATLS (Advanced Trauma Life Support), American College of Surgeons – Committee on Trauma, Students Course Manual, First Impression, 7th edition, 2002.

10)PHTLS (Prehospital Trauma Life Support, basic & advanced), Prehospital Trauma Life Support Committee of the National Association of Emergency Medical Technicians in association with The Committee of Trauma of the American College of Surgeons, 5th edition (revised), Mosby, inc, 2003.

11)ALSO (Advanced Life Support in Obstetrics), American Academy of Family Physicians, 4th edition (revised), 2006.

12)Kasper D.L., Braunwald E., Fauci A.S., Hauser S.L., Longo D.L., Jameson J.L., Harrison’s Manual of Medicine, McGraw – Hill, 16th edition, 2005.

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