This patient ingested causing cleaning products manifested by him being conscious and alert with an erythematous, ulcerated oropharynx leading to difficulty swallowing his secretions (drooling). Local contact with the caustic substance causes mucosal injury therefore, patients are conscious and alert but often have severe pain. Oropharyngeal damage leads to ulcerations and erythema. Laryngeal damage can cause hoarseness or airway compromise. Oesophageal damage can lead to dysphagia, odynophagia, and difficulty handling secretions (e.g., heavy drooling).  Gastric damage (e.g., abdominal pain) is less likely in patients with alkaline caustic ingestions, probably due to partial neutralization of the alkali by stomach acids. Full-thickness necrosis of the oesophagus can lead to perforation, resulting in either mediastinitis or peritonitis.  The most common complication are oesophageal strictures that occur weeks to months after the ingestion. Approximately one-third develop oesophageal squamous cell carcinoma years after the initial ingestion.Anticholinergic toxicity would cause xerostomia (rather than drooling), altered mental status, tachycardia, and urinary retention.  Tricyclic antidepressant toxicity often presents with anticholinergic effects, as well as mental status changes (e.g., sedation or delirium), cardiac arrhythmias, and hypotension.Ingestion of methanol results in disinhibition shortly after ingestion. Formate, a toxic substance formed after the metabolism of methanol via alcohol dehydrogenase and aldehyde dehydrogenase, is primarily responsible for the delayed (10-30 hr) symptoms of visual blurring, epigastric pain, and profound metabolic acidosis.Patients with organophosphate poisoning may have increased salivation due to cholinergic excess but typically also have bradycardia, miosis, increased urination, and diarrhoea.

Beta blocker toxicity:Symptom onset: 2-6 hr after ingestionECG findings:Prolonged PR intervalBradycardiaThis patient presented with bradycardia, hypotension, and hypoglycaemia and most likely has a beta blocker overdose, which also commonly presents with cardiogenic shock, bronchospasm, altered mental status, and seizures.  Beta blockers act as competitive antagonists for endogenous catecholamines by binding to catecholamine receptors throughout the body.  As a result, beta blockade prevents catecholamines from inducing hepatic glucose production and glycogen breakdown, which causes hypoglycaemia.Unlike other overdoses, beta blocker poisoning is diagnosed clinically based on the patient’s history and initial presentation. Virtually all patients develop symptoms within 6 hours of ingestion.  Serum levels of beta blockers are not diagnostically helpful.  Treatment consists of airway management, followed by correction of hypotension and hypoglycaemia. Intravenous fluids, atropine, and glucagon are the first-line treatment.Overdose of tricyclic antidepressants (e.g., amitriptyline) presents with altered mental status, sedation, tachycardia, and signs of anticholinergic toxicity (e.g., mydriasis, urinary retention, dry mucous membranes) without hypoglycaemia and bradycardia.Clonidine is an alpha-2 agonist used to treat hypertension. Overdose involves marked suppression of sympathetic activity and can mimic opioid overdose, presenting with bradycardia, pinpoint pupils, and altered mental status.  Although hypotension and bradycardia are seen with clonidine toxicity, hypoglycaemia is not. In addition, this patient’s 4-mm pupils make the diagnosis unlikely.Digoxin toxicity presents with nausea, vomiting, confusion, and changes in colour vision.  Patients specifically report xanthopsia, in which all objects and the environment appear yellow.  Hypoglycaemia is not typical.Bradycardia and hypotension are typical of overdose with calcium channel blockers (e.g., diltiazem)| however, altered mental status is not usually seen. Patients who overdose on calcium channel blockers have hyperglycaemia (due to impaired pancreatic insulin secretion) rather than hypoglycaemia.

Clinical experts have given guidelines to follow to estimate the amount of blood loss in road traffic accidents.Class I Haemorrhage means up to 15% of blood volume lost (up to 750 mL).Pulse rate less than 100, systolic blood pressure normal, respiratory rate is 14 to 20, urine output is greater than 30 mL/hour, mental status is slightly anxious.Class II Haemorrhage means from 15% to 30% blood volume loss (750 mL to 1500 mL). Pulse rate is from 100 to 120, systolic blood pressure normal, respiratory rate is 20 to 30, urine output is 20 to 30 mL/hour, mental status is mildly anxious.Class III Haemorrhage means from 30% to 40% blood volume loss (1500 mL to 2000 mL). Pulse rate is from 120 to 140, systolic blood pressure is decreased, respiratory rate is 30 to 40, urine output is 5 to 15 mL/hr, mental status is anxious and confused. Class IV Haemorrhage means blood loss of greater than 40% (greater than 2000 mL). The pulse rate is greater than 140, systolic blood pressure is decreased, the respiratory rate is greater than 35, urine output is negligible, mental status is confused and lethargic.This patient is suffering from class lll hemorrhagic shock.

ST-segment elevation myocardial infarction (STEMI) of the anterior wall is suspected if there is chest pain and ST elevation in leads V2 through V4. On the other hand, an irregular pulse of 120 bpm suggests atrial fibrillation (AF). AF is seen in 10-15% of the patients with acute myocardial infarction (MI) as a complication. Left ventricular failure, ischemic injury to the atria, or right ventricular infarction results in the onset of AF in the first hours of MI. Pericarditis and all conditions leading to elevated left atrial pressure can also lead to AF in association with an MI. The presence of AF during an MI is associated with an increased risk of mortality and stroke, particularly in patients who have anterior-wall MI.Urgent management of the MI takes precedence over that of AF. If the patient presents within the first 12 hours of symptoms onset, the most appropriate next step in management is reperfusion therapy either by percutaneous coronary intervention (PCI) or thrombolytic therapy with thrombolytic medications such as tissue plasminogen activator (TPA), reteplase, alteplase, tenecteplase, etc.PCI, if performed in a timely fashion (the current recommended time-to-treatment system goals acknowledge a critical total ischemic time of 120 minutes and an ideal “golden hour” of 60 minutes) and by an experienced interventional cardiologist, has better outcomes and fewer complications compared to thrombolytic therapy.AF persisting after reperfusion therapy should be managed with immediate electrical cardioversion is indicated for all patients who are hemodynamically unstable, such as those with newer worsening ischemic pain and/or hypotension. Synchronized electrical cardioversion to treat atrial fibrillation begins with 200J (or the biphasic equivalent). Conscious sedation (preferred) or general anaesthesia is advisable prior to cardioversion.A beta-blocker can be used for patients who do not develop hypotension. For example, metoprolol may be given in 5-mg intravenous boluses every 5-10 min with a maximum dose of 15 mg. Intravenous diltiazem, an alternative, should be used with caution in patients with moderate-to­ severe heart failure. In patients with new-onset sustained tachycardia (absent before MI), conversion to sinus rhythm should be considered as an option.Anticoagulation with either unfractionated heparin or low molecular weight heparin (LMWH) should be started if contraindications are absent to prevent thromboembolism.

Anaphylaxis refers to a severe systemic allergic reaction with variable features such as respiratory difficulty, cardiovascular collapse, pruritic skin rash, and abdominal cramping. It is a hypersensitivity reaction caused by an IgE-mediated reaction. Foods are the major cause in cases of anaphylaxis in which a source can be determined. Common foods that cause anaphylaxis include nuts, shellfish, and eggs.Epinephrine is the life-saving first drug of choice for patients with anaphylaxis. It should be injected as early as possible in the episode, in order to prevent progression of symptoms and signs. There are no absolute contraindications to epinephrine use, and it is the treatment of choice for anaphylaxis of any severity. The route of administration is chosen by the severity of the patient’s presentation. IV epinephrine should be administered in a patient with upper airway obstruction or hypotension. Patients with stable vital signs should receive intramuscular epinephrine instead because the risk outweigh benefit if given IV epinephrine straight. Epinephrine should be used with caution in the elderly or any patient with coronary artery disease or dysrhythmias. For patients with inadequate response to IM epinephrine and IV saline, give epinephrine continuous infusion, beginning at 0.1 mcg/kg/minute by infusion pump. Titrate the dose continuously according to blood pressure, cardiac rate and function, and oxygenation.Antihistamines, such as diphenhydramine and ranitidine, block the action of circulating histamines at target tissue receptors. Corticosteroids, such as methylprednisolone, have an onset of action approximately 4 to 6 hours after administration and, therefore are of limited value in the acute setting. However, since giving them early may blunt the biphasic reaction of anaphylaxis and therefore, it is advised to administer to patients in anaphylaxis.Though aerosolized forms of albuterol  and epinephrine are appropriate to give in the setting of anaphylaxis, they are adjunctive therapies and should never be given alone to treat anaphylaxis.

The correct answer is posterior shoulder dislocation.This pregnant patient most likely experienced a tonic-clonic seizure as suggested by a loss of consciousness accompanied by generalized shaking. She also has hypertension and proteinuria, which are findings consistent with eclampsia. Violent muscle contractions, that can occur with a seizure or electrocution injury, are common causes of posterior shoulder dislocation.In a posterior dislocation, the arm is typically held in adducted and internal rotated, with impaired external rotation, visible flattening of the anterior aspect of the shoulder, and prominence of the coracoid process. An X-ray will reveal:- Loss of the normal overlap between the humeral head and the glenoid- Internal rotation of the humeral head, leading to a circular appearance (light bulb sign) on anterior views- Widened joint space of >6 mm (rim sign) or 2 parallel cortical bone lines on the medial aspect of the humeral head (trough line sign)Potential complications associated with this type of dislocation includes fractures of the proximal humerus, labral injuries, and tears to the rotator cuff system. A majority of posterior dislocations can be managed with closed reduction.An anterior dislocation is the most common form of shoulder dislocation, typically as a result of a direct blow or a fall on an outstretched arm. Here, the patient will hold the arm slightly abducted and externally rotated.Magnesium toxicity typically presents as somnolence, loss of deep tendon reflexes, and respiratory depression, but not focal weakness. This patient’s reflexes are normal.Todd paralysis refers to a transient unilateral weakness following a tonic-clonic seizure that usually resolves spontaneously. There is no association with adduction and internal rotation of the arm.Trauma related radial nerve compression can sometimes occur in shoulder dislocations, but most commonly occurs in the forearm. It presents as weakness of wrist extension and decreased handgrip.

The patient-orientated staging of anaesthetic risk was introduced by the American Society of Anaesthesiologists (ASA). It has been helpful in categorising the degree of anaesthetic risk and proneness to morbidity prior to surgery. A prefix E can be added to each class for those having an emergency operation. The grading is associated with progressive increase in anaesthesia-related and operation-related mortality as it moves up from Class 1 (normal and healthy) to Class 5 ( unlikely to survive 24 hours with or without surgery). Patients in Classes 1-3 are usually appropriate for elective surgery where the mortality of emergency operations is double that of elective operation in Classes 1-3. There are other, more sophisticated, preoperative risk-assessment systems that are based on cardiac risk factors or on a combined points score.ASA Classification of Anaesthetic Risk Class 1: Normal healthy patients for age. Class 2: Mild systemic disease. Class 3: More severe compensated systemic disease limiting activity, but not acutely incapacitating. Class 4: Uncompensated and incapacitating systemic disease, a constant threat to life. Class 5: Patient is not expected to survive 24 hours with or without operation.The patient in this case is Class 3 given his renal disease that is well-controlled.

Opiates ( e.g. morphine, codeine, oxycodone, fentanyl and buprenorphine) overdose are commonly associated with respiratory depression, constricted pupils, bradycardia, and decreased the level of consciousness. The other clinical features (tachycardia, sweating, hypertension, and agitation) are related to sympathomimetic poisoning, some examples of which include Cocaine, Amphetamines, Ecstasy.

Acute angle closure glaucoma results from obstruction of aqueous outflow of the anterior chamber of the eye with a resulting rise in intraocular pressure as a result of a shallow anterior chamber or a chamber distorted by the development of a cataract. It occurs when a patient leaves a prolonged dimly lit situation. When the iris becomes mid-dilated, it maximally obstructs the trabecular meshwork occluding aqueous humour flow. Intraocular pressures may rise from normal (10–21 mm Hg) to levels as high as 50 to 100. Corneal oedema reduces visual acuity in the affected eye. Treatment is aimed at lowering intraocular pressure with acetazolamide, ophthalmic β-blockers, prostaglandin analogues, and pilocarpine to induce miosis. Ophthalmologic consultation and follow-up is indicated. Funduscopic examination is occasionally abnormal in acute glaucoma, but associated papilledema rarely develops acutely. Corneal examination with fluorescein is used to diagnose corneal abrasions or other corneal pathology (i.e., ulcers, keratitis, foreign body, corneal rupture). The cornea may appear normal or “steamy” in the setting of acute glaucoma as the edges accumulate oedema from the increase pressure of the anterior chamber. The cornea should not take up fluorescein. LP is used to diagnose intracranial pathology. The acute unilateral pain of glaucoma may make the clinician consider a SAH, but glaucoma should always be considered. A change in visual acuity is nonspecific and should not be a diagnostic for glaucoma

This is a case of suspected paracetamol toxicity due to there presenting symptoms of RUQ pain or tenderness, nausea, vomiting thus, she should be given N-acetyl cysteine (NAC) intravenously immediately. As this is ordered, obtain a blood sample for serum paracetamol level + ALT ( alanine aminotransferase). However, the results would not be available until ≥ 8 hours after ingestion thus, NAC can be safely stopped if the paracetamol level is within the safe range and continued if it is in the toxic range. Management for paracetamol poisoning is summarized as below:Cooperative adult patients who have potentially ingested ≥ 10 g or ≥ 200 mg/kg (whichever is less). – For paracetamol ingestions ≥ 30 g, activated charcoal should be offered until 4 hours after ingestion. – If paracetamol concentration will not be available until ≥ 8 hours after ingestion, commence acetylcysteine while awaiting paracetamol concentration. Further assessment is required if they develop abdominal pain, nausea or vomiting.

Intramuscular adrenaline 500 micrograms 1:1000 should be given immediately to prevent shock and respiratory compromise in this patient that developed signs and symptoms of anaphylaxis (breathing difficulty plus facial oedema after eating a coffee cake). This patient is also high risk for anaphylaxis due to the history of asthma.If airway oedema is not responding to parenteral and nebulised adrenaline, early intubation is indicated.Corticosteroids, antihistamines and anti-leukotrienes have no proven benefit on the immediate and life-threatening anaphylaxis. Review of Anaphylaxis symptoms systemically:-Respiratory features:Tongue swelling, stridor, hoarse voice or change in the character of the cry, tightness or tingling in the throat, persistent cough, wheeze, subjective feeling of tightness chest/throat.-Cardiovascular features:Palpitation, altered consciousness/confusion, tachycardia, bradycardia, hypotension, cardiac arrest.-Gastrointestinal features:Nausea, vomiting, diarrhoea, abdominal/pelvic pain.-Mucocutaneous features:Generalized pruritus, urticaria/ intense erythema, conjunctival erythema and tearing, flushing, angioedema.-Neurological Features:A headache, dizziness, confusion, collapse with or without unconsciousness.

The resuscitation team should immediately be called in cases of collapsed patients. Perform uninterrupted chest compressions while monitoring pads are applied. Immediate defibrillation is the best treatment for monomorphic ventricular tachycardia. Vtach and Vfib both require urgent defibrillation.

Although this patient has developed a mild headache, he has no loss of consciousness and intracranial bleeding has been ruled out with his negative CT brain and lumbar puncture thus, this patient can safely be discharged home with head injury advice. Advise patient to return to the hospital if any symptoms of raised intracranial pressure such as worsening of headache, nausea, vomiting, and changing of the level of consciousness.

The best first line of management is to administer 1 ml of 1 in 1,000 adrenalines (1mg) subcutaneously.The patient’s presentation is indicative of a severe life-threatening anaphylaxis to a bee sting.The intravenous route for administration of adrenaline is preferred, but in this case, the subcutaneous route is more practical.Adrenaline helps maintain blood pressure, counteracts the effects of the released mediators, and inhibits further release of mediators.The insertion of a central venous catheter is not indicated in this case.Intravenous plasma-expanding solutions (e.g. gelatin solution) could be necessary after initial adrenaline treatment, and is normally administered via a peripheral venous line.High flow oxygen and nebulised salbutamol are indicated during emergency care of anaphylaxis with associated respiratory obstruction, but after administration of adrenaline.Anaesthesia and intubation are not indicated in this case.

The most likely diagnosis would be a perforated oesophagus, as supported by his history of being an alcoholic, his symptoms of shock, hypotension, peripheral cyanosis and chest findings consistent with a fluid collection following the vomiting. The presence of chest pain with sudden onset following vomiting should be a red flag. Projectile vomiting against a closed glottis (when the patient tries to hold it in) is a typical feature. An oesophageal perforation as a consequence of elevated intraoesophageally pressure, leading to spillage of gastric, oesophageal fluid and gases into the mediastinum and the pleural space, commonly the left side. Confirmation of the diagnosis can be done by looking for the presence of any oesophageal perforation via CECT (a contrast-enhanced CT) of the neck and thorax. If that cannot be done, a conventional contrast study can prove to be helpful as well. It is contraindicated to carry out an endoscopy before any imaging has been done to avoid conversion of a partial tear into a complete one and forcing more gastric spillage into the chest. Once resuscitation and confirmation of the diagnosis have been done, the next steps would be to repair the perforation and address the spillage. If the perforation if found to be a few days old and the fluid collection is contained, intervention is unnecessary. However, open thoracotomy debridement along with oesophageal tear approximation as well as chest cavity drainage should be done if the patient is found to have gross spillage of gut contents in the chest. In order to prevent progression into septic shock (which could be fatal), mediastinitis and pneumonitis, the repair and sealing of the perforation has to be done along with simultaneous aggressive antibiotics. Pleural drainage may also be needed. The oesophageal tear can either be sealed by endoscopic stenting or open surgery. The presence of any subcutaneous emphysema either in the neck, chest or abdomen as well as mediastinal emphysema should be looked out for, both of which are also diagnostic features of the condition.A perforated peptic ulcer typically presents with symptoms of upper abdominal pain and tenderness that are sudden in onset along with board-like rigidity. However, vomiting is usually absent. Imaging of the patient sitting in an upright position would be able to show gas below the diaphragm. Epigastric pain that is sudden in onset can also occur in acute pancreatitis. It is often associated with prostration and profuse vomiting. Patients often have a history of heavy alcohol abuse, such as this patient. On examination, there may be evidence of left lung base abnormalities. However, mediastinal and subcutaneous emphysema would not be expected as in oesophageal rupture. Pancreatitis can result in lung complications such as pleural effusion and atelectasis. Elevated serum amylase and lipase are frequently observed. Spontaneous pneumothorax can present as chest pain and dyspnoea of sudden onset. If it is large enough, it can produce the classical features of hyperresonance. Breath sounds would also be absent on the affected side. Chest imaging would be able to confirm this diagnosis. However, it is less likely to be the diagnosis in this case as abdominal signs are not expected in this condition. Myocardial infarction often presents with chest pain of an acute onset and can appear similar to acute upper abdominal emergencies but the history would often give evidence supporting a cardiac cause such as the ECG changes and findings on cardiac examination. Major chest findings with only a unilateral involvement such as those described in the vignette would be absent.

In the past, lead was added to petrol and household paints. The hazardous small particles of lead can be taken into the body by swallowing or breathing. Lead exposure can come from lead-based household paints which were used before 1970, old household pipes, and household dust which may contain lead particles from deteriorating or incorrectly removed lead-based household paint. Less commonly, lead exposure can occur form contaminated soil or dust brought into the house from shoes.The symptoms of lead poisoning depend on the degree and length of exposure. The most common symptoms may include anaemia, loss of appetite, irritability, fatigue, abdominal pain, nausea, vomiting, ataxia, muscle weakness, and seizures. A common lab finding of chronic lead poisoning is basophilic stippling of red blood cells.Mercury poisoning is associated with the consumption of contaminated fish. There are also specific professions that may have been exposed, notably dentists who recovered the mercury from old amalgam fillings and in the millinery (hat) industry when mercury was used in the manufacturing process of felt hat blocking. Chronic mercury poisoning causes central nervous system toxicity that presents as intention tremor, excitability, memory loss, and delirium.Arsenic poisoning is a favourite of crime novelists as it is tasteless and colourless when added to food or drink. Chronic arsenical poisoning causes skin rashes and gastrointestinal symptoms.Carbon monoxide poisoning was a potential problem with old gas heaters. Usually, it would occur during the colder months in areas that rely on older heaters. Also, it was an issue in areas where hot water was heated and people would die of carbon monoxide poisoning in the shower due to a lack of ventilation. In the past, iron poisoning used to come from cooking in iron pots and would cause secondary haemochromatosis.

This is a suspected suicide attempt using a cleaning fluid containing carbon tetrachloride, a potent hepatic toxin. She developed fetor hepaticus, a distinctive smell to her breath that reflects a profound metabolic disturbance as hepatic damage progressed. As liver function declined, the serum ammonia level rose. The triphasic waves typically seen in hepatic encephalopathy may occur with uraemia and other causes of metabolic encephalopathy.

The correct answer is 4.8 litres of fluid in first 24 hours and 2.4 litres has to be given in first 8 hours.Fluid volume and rate of IV fluid requirements in the first 24 hours after a burn are determined by the Parkland formula which is:4 mL/kg/percentage of total body surface area burnedIn this case, it would be:4 x 80 x 15 = 4800mLThe appropriate fluid recommended for this case is lactated Ringer solution (Hartman).

Anticholinergics (e.g. tricyclic antidepressants, antihistamines, and benztropine), when overdosed, manifests as agitated delirium, tachycardia, visual hallucinations, hyperthermia, dilated pupils, dry flushed skin, urinary retention, and constipation. Opiates (e.g. morphine, codeine, oxycodone, fentanyl and buprenorphine) overdose manifest as respiratory depression, constricted pupils, bradycardia, and decreased the level of consciousness.

Pulseless electrical activity (PEA) management includes starting CPR (30:2) immediately, securing an airway and providing intravenous access. IV adrenaline should be given if not responsive,. Looking for a correctable cause of PEA and correcting that is always an important part of management.Defibrillation has no role in management of PEA as the organized electrical activity of the heart is preserved. There is no recommendation to support the use of atropine in PEA or asystole.