Emergency Medicine Final Exam Notes PDF

Sigrún Lilja EMERGENCY MEDICINE FINAL EXAM NOTES 1 1. A. The unconscious patient (differential diagnosis) B. Acute CO and CO2 poisoning 2. A. Acute respiratory failure (causes, types, treatment) B. Organophosphate poisoning (mechanism, clinical features, treatment) 3. A....

Sigrún Lilja EMERGENCY MEDICINE FINAL EXAM NOTES 1 1. A. The unconscious patient (differential diagnosis) B. Acute CO and CO2 poisoning 2. A. Acute respiratory failure (causes, types, treatment) B. Organophosphate poisoning (mechanism, clinical features, treatment) 3. A. Head injuries (age-specific mechanisms, localization, complications, clinical features, treatment) B. Opioid poisoning (mechanism, clinical features, antidote, treatment) 4. A. Pediatric basic and advanced life support (PBLS, PALS) B. Differential diagnosis of chest pain 5. A. Acute left heart failure (mechanism, etiology, clinical features, treatment) B. Pneumothorax, hemothorax (diagnosis, treatment) 6. A. Treatment of acute respiratory failure in children (croup, acute asthma, foreign body aspiration) B. Delivery on the spot (technique, complications, atonia, uterine rupture, limb presentation, breech presentation) 7. A. Surgical emergencies: acute appendicitis, acute pancreatitis, duodenal ulcer, peptic ulcer disease, perforation B. Airway management (airway opening maneuvers, equipment, indications and contraindications of NIV) 8. A. Surgical emergencies: peritonitis, acute cholecystitis, ileus B. Bronchial asthma (pathomechanism, types, clinical features, treatment) 9. A. Diagnosis and treatment of rhythm abnormalities (atrial fibrillation and flutter) B. Differential diagnosis of headache 10. A. Shock (types, treatment, cardiogenic and hemorrhagic shock) B. Mushroom poisoning (types, treatment, Amanita phalloides poisoning) 11. A. Acute coronary syndrome (clinical features and treatment) B. Hypothermia (causes, pathomechanism, clinical features, treatment) 12. A. Junctional tachycardias (AVRT and AVNRT) B. Sepsis (pathomechanism, clinical features, treatment) 13. A. Preexcitation syndromes (WPW, LGL) (clinical features, diagnosis, treatment) B. Scoring systems in emergency medicine (Wells score, CURB65, ChadVasc score, Glasgow Coma Scale, Wallace rule, SOFA score) 2 14. A. Pulmonary embolism (diagnosis, treatment) B. Airway obstruction (types, clinical features, treatment) 15. A. Fits and seizures in children (causes, diagnosis, treatment) B. Hypertensive problems (pathomechanism, diagnosis, treatment, complications) 16. A. Stroke, subarachnoid haemorrhage, intracranial bleeding (diagnosis, treatment) B. Allergies and anaphylaxis (pathomechanism, clinical features, treatment) 17. A. Epilepsy in adults (causes, types, treatment) B. Burns (types, classification, diagnosis, treatment) 18. A. Atrioventricular conduction abnormalities, diseases of the sinus node (clinical features, diagnosis, treatment) B. DVT (causes, clinical features, diagnosis, treatment) 19. A. Heat illness (heat cramps, heat exhaustion, heat stroke – pathomechanism, clinical features, treatment) B. Benzodiazepine poisoning (pathomechanism, clinical features, treatment) 20. A. Ventricular rhythm abnormalities (extra beats, tachycardias – causes, types, diagnosis, treatment) B. Penetrating and non-penetrating chest injuries (commotio cordis, cardiac tamponade, lung injuries, pneumothorax, haemothorax, aortic rupture – diagnosis, treatment) 21. A. Penetrating and non-penetrating abdominal injuries B. Cardiac arrest (causes, CPR, BLS, BLS/AED) 22. A. Pelvic injuries (diagnosis, treatment) B. Ethylene glycol, methanol and ethanol poisoning 23. A. ALS B. General principles of poisoning (antidotes, indications/contraindications and ways of invasive/non-invasive treatment) 24. A. Endocrine emergencies (hypoglycaemia, hyperglycaemic crises, diabetic ketoacidosis, thyrotoxic and Addisonian crisis) B. Beta-blocker, digoxin and calcium antagonist poisoning 25. A. GI bleeding (clinical features, treatment) B. Peri-arrest arrhythmias (causes, diagnosis, treatment) 26. A. Polytrauma – general principles (International Trauma Life Support, ITLS) B. Triage (general principles) 3 27. A. Pneumonia (pathomechanism, classification, clinical features, diagnosis, treatment) B. Arterial and venous bleeding (clinical features, medical therapy and mechanism of action) 28. A. COPD (pathomechanism, clinical features, treatment) B. Fever (pathomechanism, treatment in adults and children) 29. A. Acute and chronic right ventricular failure (causes, clinical features and emergency treatment) B. Bedside diagnostic in emergency medicine (Point of Care) 30. A. Disturbances of consciousness, changed mental status (somnolence, sopor, coma, delirium) B. The base patomechanism of emergency treatment (ABCDE approachment) 4  1. A. The unconscious patient (differential diagnosis) B. Acute CO and CO2 poisoning Being unconscious refers to the lack of awareness and capacity for sensory perception. It can be objectively measured with the help of the Glascow coma scale. It can have many causes so history taking (heteroanamnesis) is important to be able to distinguish between them because treatments may vary depending on the cause. Treament may be needed before diagnosis in some cases. Differential diagnosis of unconsciousness Common causes: Uncommon causes: Hypoglycaemia Type 2 respiratory failure Drug overdose Cardiac failure Head injury Arrhythmias Stroke Hypovolaemic shock Subarachnoid haemorrhage Anaphylaxis Convulsions Hepatic/renal failure Alcohol intoxication Hypothermia/hyperthermia Meningitis/encephalitis Malaria DKA/HHS Non-convulsive status epilepticus Wernicke’s encephalopathy Remember Airway, Breathing, and Circulation. Assess level of consciousness using GCS. Check the blood glucose and treat hypoglycaemia immediately. Record pupil size. Give slow IV thiamine to patients with a history of alcoholism or who appear malnourished. History Ask form ambulance crew, family/friends: How was the patient found? When was he/she last seen? Is there any suggestion of trauma? Is there any history of fits? Has there been recent foreign travel? Previous symptoms and medical history (including depression). Note any drugs available. 5 Examination Check for illness/injury. Check clothes/possessions for drugs or cards/bracelets for pre-existing disease. Increased respiratory rate may reflect airway obstruction, aspiration, pneumonia, DKA, liver/renal failure, salicylate poisoning, methanol, or ethylene glycol. Respiratory depression may be due to poisoning (e.g., barbiturates, opioids, tricyclics), or increased ICP. Brainstem compression or damage by stroke may cause rapid, irregular or intermittent (Cheyne-Stokes) breathing. If bradycardic consider: hypoxia, complete heart block, increased ICP, digoxin or β- blocker poisoning. If tachycardic consider: airway obstruction, hypoxia, hypovolaemia, SVT, VT, or anticholinergic overdose. AF may be associated with cerebral emboli. Hypotension suggests hypoxia, shock (hypovolaemic, anaphylactic, septic), or poisoning. Hypertension may be due to increased ICP. Skin: look for pallor, cyanosis, jaundice, spider naevi, skin crease/scar, pigmentation (Addison’s disease), rash (e.g., purpura in meningococcal infection or DIC), injection marks (drug addiction or medical treatment), and signs of trauma. Erythema or blistering over pressure points indicates that the patient has been unconscious for some hours. Measure temperature (rectal). Hypoglycaemia can cause localized weakness/coma and mimic stroke. TCAs often cause coma with dilated pupils, a divergent squint, increased muscle tone, jerky limb movements, and extensor plantars (Babinski) Coma with small pupils and respiratory depression suggests opioid poisoning. Psychogenic coma: Patients sometimes pretend to be unconscious. It can be difficult to be certain of this–exclude other causes first. Suspect psychogenic coma if serious pathology has been excluded and when the eyes are open, only the sclera shows the eyes deviates upwards (Bell’s phenomenon). Little extra info on assessing consciousness. Glascow coma scale: AVPU scale: Verbal, motor and eye-opening response Alert, Voice, Pain, Unresponsive to stimuli are measured, scored and A system to measure and record patients added into a final score on a scale of 3-15. responsiveness, indicating their level of Lower score are associated with a more consciousness. decreased level of consciousness. 6 1B. Carbon monoxide and carbon dioxide poisoning Carbon monoxide poisoning CO is a tasteless and odorless gas. Poisoning may occur from car exhausts, fires, and faulty gas heaters. CO decreases the oxygen-carrying capacity of the blood by binding Hb to form carboxyhemoglobin (COHb). This impairs oxygen delivery from blood to the tissues and also inhibits cytochrome oxidase, blocking oxygen utilization. Causes severe hypoxia. Clinical features: headache, malaise, nausea, vomiting In severe poisoning: coma with hyperventilation, hypotension, increased muscle tone, increased reflexes, extensor plantars and convulsions. Cherry-red coloring of the skin may be seen in fatal CO poisoning, but is rare in live patients. Skin blisters and rhabdomyolysis may occur after prolonged immobility. Pulmonary edema, MI and cerebral edema can occur. Management: Remove from exposure Clear the airway and maintain ventilation with as high a concentration of oxygen as possible Record ECG and monitor heart rhythm Check arterial blood gases à hypoxia Check COHb levels. COHb >15% after arrival at hospital suggests serious poisoning Correct metabolic acidosis by ventilation and O2: try to avoid bicarbonate, which may worsen tissue hypoxia Consider mannitol if cerebral edema is suspected Carbon dioxide poisoning 7  2. A. Acute respiratory failure (causes, types, treatment) B. Organophosphate poisoning (mechanism, clinical features, treatment) Acute Respiratory Failure Definition: Acute impairment in gas exchange between the lungs and the blood causing hypoxia with or without hypercapnia. The cause of respiratory failure can be mechanical insufficiency of the breathing or alveolo-capillary dysfunction. It is not an independent entity; it is always a consequence of various pathologic processes. There are 2 types: Hypoxic respiratory failure (type 1 respiratory failure) is hypoxia without hypercapnia and with an arterial partial pressure of oxygen (PaO2) of 50 mmHg. Hypoxemia is common in pts with hypercapnic respiratory failure. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders; asthma and chronic obstructive pulmonary disease (COPD). In type 2 failure the patient may develop life-threatening respiratory failure if administered 8 high concentrations of oxygen! Aim to maintain SpO2 at 88–92%, and recheck ABGs in 30 min. How to differentiate between acute and chronic type 2 respiratory failure? Patients who normally have a slightly increased pCO2 will also show increased HCO3 on ABG. The kidneys adapt over a period of days to retain bicarbonate, in attempt to buffer the respiratory acidosis. Regarding perfusion abnormalities remember the layers the gases need to pass through: Surfactant à Alveolar epithelium à basement membrane à capillary endothelium à plasma à RBC membrane à intracellular fluid à into the Hb molecule Disruption occurring along these barriers would surely cause impairment. Pulmonary Causes of perfusion abnormalities: Perfusion = delivery of oxygenated blood to tissues Acute Lung Injury, Acute Respiratory Distress Syndrome (ALI/ARDS) Acute bronchospasm – severe asthma Acute on chronic airflow limitation acute exacerbation of COPD Severe pneumonia Pulmonary embolism Pulmonary edema Aspiration, inhalation Causes of ventilation problems: Ventilation = moving air in and out of lungs, facilitating gas exchange; bringing in O2 and flushing out CO Central: CNS – spinal cord Injuries (C3,4,5 for phrenic nerve which innervates the diaphragm, and lower levels for intercostal muscles) Note: Accessory resp. muscles are only used under conditions of high metabolic demand (e.g. exercise) or respiratory dysfunction (e.g. an asthma attack). Drug action: e.g. Opioids. Neurologic, neuromuscular, muscular failures: e.g. Myasthenia gravis, Guillain Barré syndrome, muscle relaxants. Mechanical causes: Thoracic cage: rib fractures, burns, scars etc. Compression of the lungs: hydrothorax, hemothx, pneumothx Airway obstruction o Tongue(most common) o Foreign body obstruction o Anaphylaxis/angioedema/ laryngeal angioedema! o Upper airway burns o Maxillofacial/laryngeal/tracheobronchial trauma o Epiglottitis o Croup 9  Upper airway obstruction: more likely foreign body, stenosis etc. Lower airways: more likely bronchospasm, asthma etc. Problems in the lung parenchyma itself Clinical signs of respiratory insufficiency Dyspnea Use of accessory muscles of respiration Cyanosis Progressive elevation of the resp. rate (tachycardia) Agitation, confusion, somnolence, coma Assessment of the patient Airway: Listen to the patient talk/breathe Noisy breating = Obstructed breathing (but not all obstructed breathing is noisy) Adventitious sounds o Snoring = tongue o Stridor = tight upper airway Breathing: Look o Symmetry of chest expansion o Signs of increased effort o Skin color Listen o Mouth and nose o Lung fields Feel o Mouth and nose o Symmetry of expansion Respiratory patterns o Cheyne-Stokes: diffuse cerebral cortex injury o Kussmaul: acidosis o Biot‘s (cluster): Increased ICP; pons, upper medulla injury o Central neurogenic hyperventiclation: Increased ICP; mid-brain injury o Agonal: shallow, slow, irregular breathing: brain anoxia. Tachypnea Bradypnea Signs of distress o Nasal flaring, tracheal tugging, retractions, accessory muscle use, tripod positioning Cyanosis 10 Circulation: Don‘t let respiratory failure distract you! Tachycardia = early hypoxia in adults Bradycardia = early hypoxia in infants and children, late hypoxia in adults. Focused exam: Neck: Trachea in midline? Jugular vein distension? Subcutant emphysema? Accessory muscle use? Hypertrophy? Chest: Barrel chest? Deformity, discoloration, asymmetry? Flail segment, paradoxical movement? Adventitious breath sounds? 3rd heart sound? Subcutant emphysema? Fremitus? Dullness, hyperresonance during percussion? Extremities: Edema? Nail bed color? Clubbing? Disability: Restlessness, anxiety, combativeness = hypoxia until proven otherwise. Drowsiness, lethargy = hypercapnia until proven otherwise Attention, when the fighting stops, the patient isn‘t always getting better! Diagnosis Inspection: dyspnea, thoracic movements, etc. Respiratory rate Pulse-oximetry Blood gases (arterial, venous) – repeated! Reaction to oxygen inhalation (consider perfusion abnormality if no improvement) Asthma: peak flow Further investigations Thorax X ray, CT, MRI Sputum - bacteriology, serology Laboratory testing ECG, US (TEE?) 11 12 Acute lung injury/ Acute respiratory distress syndrome (same thing don’t get confused) ARDS is an acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue. Clinical hallmarks of ARDS are hypoxemia and bilateral radiographic opacities, while the pathological hallmark is diffused alveolar damage (alveolar edema with or without focal hemorrhage, acute inflammation of the alveolar walls, and hyaline membranes). Reduced ventilated lung-capacity Reduced compliance Severe hypoxemia (intrapulmonary shunts) o Intrapulmonary shunts: the passage of deoxygenated blood from the right side of the heart to the left withot partaking in gas exchange in the pulmonary capillaries. A pathological condition that results when the alveoli of the lungs are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region. Often occurs when alveoli are filled with fluid. Diagnosis: Chest X ray/ CT Severe hypoxia – not reacting on oxygen inhalation PaO2/FiO2 < 300 (ALI) or 200 (ARDS) o PaO2/FiO2 ratio (Horowitz index) is a comparion between the O2 level in the blood and the O2 concentration that is breathed. This helps determine the degree of any problem with how the lungs transfer oxygen to the blood. A ratio of < 200 is necessary for the diagnosis of ARDS. Decreased lung compliance. Diffuse bilateral infiltration not caused by LV insufficiency (Paop 18 Hgmm) Causes of ALI/ARDS Pulmonary: Extrapulmonary: Infection/pneumonia Sepsis Aspiration/inhalation Trauma Near drowning TRALI (transfusion related acute Contusion lung injury CPB (cardiopulmonary bypass) Treatment should go according to the underlying cause of the condition. So the most important focus should be in assessing the current situation and supporting the patient until an underlying cause is found and then treating accordingly. 2B. Organophosphate poisoning Organophosphates are widely used as insecticides (e.g. Parathion). They are absorbed through the skin, bronchial mucosa and gut, and inhibit cholinesterases, causing accumulation of ACh at nerve endings and NMJs. Irreversible binding of acetylcholinesterase (“ageing”) develops after some minutes or hours, leading to an increase in Ach and a life-threatening activation of the PNS. 13 Pralidoxime reactivates cholinesterase if given promptly, before ageing occurs. Clinical features: Acute cholinergic crisis Early features: Anxiety, restlessness, insomnia, tiredness, headache, nausea, vomiting, abdominal colic, diarrhea, sweating, hypersalivation, and miosis. Muscle weakness and fasciculation may develop. In severe poisoning: Widespread paralysis with respiratory failure, pulmonary edema, profuse bronchial secretions, bronchospasm, convulsions, and coma. Hyperglycemia and cardiac arrhythmias may occur. Occasionally, delayed effects of poisoning develop 1-4 days after acute poisoning, with cranial nerve palsies, muscle weakness and respiratory failure which resolve after 2-3 weeks. A peripheral neuropathy may develop after 2 weeks, usually involving the legs. Management: Wear protective clothing Give supportive treatment Clear the airway and remove secretions. Give O2. Measure erythrocyte cholinesterase activity. If there are profuse bronchial secretions or bronchospasm, give atropine IV. o Atropine is a competitive antagonist at muscarinic Ach receptors. Give diazepam to treat agitation and control convulsions. Pralidoxime 14  3. A. Head injuries (age-specific mechanisms, localization, complications, clinical features, treatment) B. Opioid poisoning (mechanism, clinical features, antidote, treatment) Common causes of head injuries Road traffic collisions of all types Falls Assaults Sporting and leisure injuries Workplace injuries Primary injury occurs at the time of the head injury. This takes the form of axonal shearing and disruption, with associated areas of hemorrhage. This primary damage may be widespread (“diffuse axonal injury”) or localized (eg “contre-coup” frontal contusions in a fall hitting the occiput). Secondary injury occurs later, due to various problems that commonly co-exist. Many of these are preventable or treatable, and should thus be the focus during resuscitation: Hypoxia Hypovolemia and cerebral hypoperfusion Intracranial hematoma with localized pressure effects and increased ICP Other causes of increased ICP, including cerebral edema and hypercapnia Epileptic fits Infection Increased ICP leads to a reflex increase in systemic arterial BP together with bradycardia: this combination is the Cushing response (or vasopressor response). Head trauma Soft tissues: Horristic bleeding Hematoma Facial fractures: Nose: epistaxis, tumefaction (swelling) Mandibula: stair-sign on tooth, rare airway obstruction Maxilla Zygomatic arch Basilar skull fractures: Anterior scala: mixture of blood and CSF flows from nose, uni- or bilateral periorbital ecchysmoses („raccoon eyes“). Medium scala: Mixture of blood and CSF flows from ears, impaired hearing. Posterior scala: pharyngeal hematoma or mixture of blood and CSF in pharynx, mastoid ecchysmoses, subcutant emphysema in the neck. Cerebral injuries: Concussion: loss of consciousness, which returns in 15 min. Later amnesia, headache, dizziness, nausea. No irriversible neurologic deficit. Contusion: longer loss of consciousness, sometimes irreversible hemi-signs (fx. Anisocoria), signs of increasing ICP. 15  Epidural hematoma: Injury to middle meningeal artery. Rapid process. Massive increasing ICP signs: mostly caused by mass effect, results of local injury (hemi signs). Subdural hematoma: Injury to bridging veins. Mostly slower progression, lucid interval. Intracerebral hematoma: both massive hemi and diffuse signs. Fast progression. Secunder cerebral lesion: caused by O2 deficiency and/or perfusion failure. Linked with serious head trauma. Markedly increased mortality. Indications for referral the hospital Impaired consciousness level at any time Amnesia for the incident or subsequent events Neurological symptoms (vomiting, severe and persistent headache, seizures) Clinical evidence of a skull fracture (CSF leak, peri-orbital hematoma) Significant extracranial injuries Worrying mechanism (high energy, possible non-accidental injury, possible penetrating injury) Continuing uncertainty about the diagnosis after first assessment. Medical co-morbidity (anticoagulant use, alcohol abuse) Adverse social factors (e.g. alone at home) Imaging: CT, MRI, X-ray Initial management Clear, establish, and maintain the airway; provide O2; protect the cervical spine Check breathing—provide support as necessary Check blood glucose and treat hypoglycemia if present FBC, clotting screen, U&E (urea + electrolytes) Correct hypovolemia, resuscitate, and treat other injuries Give IV antibiotics for patients with compound skull fractures Clean and close scalp wounds to control scalp bleeding Insert a urinary catheter Consider the need for tetanus immunization 3B. Opiate overdose, poisoning The opioids include morphine, diamorphine (heroin), pethidine, codeine, buprenorphine, nalbuphine, methadone, diphenoxylate, and related drugs. These are used as analgesics, cough suppressants, and anti-diarrheal agents. Acute opioid poisoning often occurs in addicts. Clinical features: Coma Decreased respiratory rate Pinpoint pupils Sometimes cyanosis, apnea, convulsions, and hypotension. 16 Respiratory depression may cause death within 1 hour of an opioid overdose. Delayed toxicity may occur with slow-release formulations of drugs, and also with methadone, which has a very long duration of action (half-life 25-50 hours). Treatment: Clear and maintain the airway Ventilate on O2 with a bag mask or ET tube. Naloxone is a specific antagonist for opioids and reverses coma and respiratory depressions if given in sufficient dosage. Naloxone has a much shorter duration of action than most opioids and so coma and respiratory depression often recur when naloxone wears off. In opioid addicts, naloxone may precipitate a withdrawal syndrome with abdominal cramps, nausea, and diarrhea, but these usually settle within 2 hrs. Ventricular tachyarrhythmias occur occasionally. 17  4. A. Pediatric basic and advanced life support (PBLS, PALS) B. Differential diagnosis of chest pain Pediatric basic life support (PBLS) 18 Pediatric basic life support: Ensure safety Check responsiveness Gently stimulate and ask „are you allright?“ Answering and moving: leave in position, check condition and get help. Re-assess. Shout for help Open the airways Head tilt – chin lift Jaw thrust Keep airway open, check breathing for 10 sec. If breathing: recovery position, get help and re-assess Absence of breathing: remove any obvious airway obstruction Give 5 initial rescue breaths Assess circulation No more than 10 sec Look for signs of life: movement, coughing, breathing Check the pulse (professionals) o > 1 year old: carotid or femoral pulse o < 1 year old: brachial or femoral pulse If there are no signs of life Start chest compressions Combine with rescue breaths Chest compressions: 100-120/min Lower half of sternum 1/3 deep of the AP chest diameter (or 4-5 cm) > 1 year old: 1 or 2 hand technique < 1 year old: 2 fingers (alone) or encircling way. Continue CPR until: The child shows signs of life Further qualified help arrives Exhaustion 19 Advanced pediatric life support: Pediatric advanced life support During CPR: Ensure high quality CPR: rate, depth, recoil Plan actions before interrupting CPR Give O2 Vascular access: intravenous, interosseus Give adrenalin every 3-5 min Consider advanced airway and capnography 20  Continuous chest compressions when intubated Correct reversible causes Reversible causes (4H/4T) Hypoxia Tension pneumothorax Hypovolemia Toxins Hypo-/hyperkalemia Tamponade (cardiac) Hypothermia Thromboembolism 21 Pediatric CPR doses Fluids: Isotonic crystalloids 20 ml/kg Adrenalin 0.01 mg/kg every 3-5 min Amiodarone VF or pulseless VT After 3rd and 5th shock give 5 mg/kg Calcium Hypocalcemia Calcium channel blocker overdose Hypermagnesemia Hyperkalemia Glucose Only in hypoglycemia Magnesium Hypomagnesemia or Torsade de Pointes 50 mg/kg Sodium bicarbonate Not given routinely Hyperkalemia TCA overdose 4B. Differential diagnosis of chest pain Always take chest pain seriously. It may reflect life-threatening illness. Chest pain could arise due to a variety of different causes, and it is important to diagnose whether it is a serious urgent cause that requires fast care, or a benign cause that doesn’t require a lifesaving treatment. History is essential! Characterize the pain Site: e.g central(substernal), bilateral or unilateral Severity: scale of 1-10 Time of onset and duration. Character: e.g. ‘stabbing’, ‘tight/gripping’, or ‘dull/aching’ Radiation: e.g to arms and neck in myocardial ischemia. Precipitating and relieving factors: e.g. exercise, rest, GTN spray Previous similar pains. Enquire about associated symptoms Document past history, drug history, and allergies. Old notes and old ECGs are invaluable so request them at an early stage. 22 Examples of non-cardiac causes of chest pain: Sharp stabbing pain could be due to pleuritis, pericarditis (accompanied by a pericardial rub sound). One sided strong pain could be pneumothorax ( non-MI emergency), accompanied by dyspnea. If it increases with inhaling or exhaling, most likely non-cardiac in origin, specifically chest wall problem. Could be tender to the touch, which is for sure non cardiac in nature! Stress can cause left sided chest pain, with also radiation to arm. Here asess duration of the chest pain and you may as well exclude cardiac origin with help of ECG and blood test. GERD. Very common and occurs following a meal; sharp substernal pain. Extremely painful sharp stabbing pain retrosternal is can be due to aortic dissection, which is a non-MI emergency. Exertional Angina: Episodic pain, 20 min o High risk of AMI Pulmonary embolism: Atypical, presenting with any combination of: o Chest Pain, dyspnea, syncope, shock, hypoxia o Fever, cough, hemoptysis Pain is often pleural o Reproducible with breathing, palpation Classic presentation: o Sharp pain, dyspnea o Tachypnea, tachycardia, hypoxemia Aortic Dissection: Risk Factors: Atherosclerosis, HTN (uncontrolled), coarctation of aorta, bicuspid aortic valve, aortic Stenosis, Marfan Syn, Ehlers-Danlos Syn, pregnancy Pain: midline Substernal chest pain, tearing, ripping, searing, radiating to interscapular area Pain above and below diaphragm Often associated with stroke, AMI, limb ischemia Spontaneous Pneumothorax: Risks: o Sudden change in barometric pressure o Smokers, COPD Pain: o sudden, sharp, pleuritic chest pain, and dyspnea Dianosis: o Absence of breath sounds ipsilaterally o Hyperresonance to percussion o Chest x ray Esophageal Rupture (Boerhaave Syn): Life-threatening Substernal, sharp chest pain Sudden onset after forceful vomiting Dyspneic, diaphoretic, and ill-appearing Chest x ray: Normal, pleural Effusions, pneumothorax, pneumoperitoneum, pneumomediastinum Water soluble contrast Study 24 Acute Pericarditis: Acute, sharp, severe, constant, substernal CP Radiation to back, neck, shoulders Worse with lying down and inspiration Relief with leaning forward FRICTION RUB EKG: ST segment elev., T wave inversion, or PR depression Mitral Valve Prolapse: Women > Men Discomfort at rest Associated symptoms: Dizziness, hyperventilation, anxiety, depression, palpitations, fatigue, SVT, ventricular dysrhythmia Tx: Beta-Adrenergic Blockers Diagnosis: Echo GI Disorders: GERD/dyspepsia Burning chest pain Acidic taste Recumbent position increases pain Relief per antacids. CAREFUL, can also help in ACS Esophageal Spasm: Sudden onset, dull, tight, gripping Hot or cold liquids Large food bolus Responds to NTG Peptic Ulcer Disease: Gastric: Postprandial, dull, boring pain Mid-epigastric, may awake pt. Duodenal Ulcer: Relieved after eating Symptomatic Tx: antacids DDx: Pancreatitis and Biliary tract disease Panic Disorder: Recurrent, unexpected panic Including at least 4 SX: o Palpitations, diaphoresis, tremor, dyspnea, choking, chest pain, nausea, dizziness, derealization, or depersonalization,fear of losing control or dying, paresthesias, chills, hot flashes Rule out substance abuse Proper history taking is very important. Ask all the questions but don’t waste time. 25 For the chest pain to be caused by an MI/acute coronary syndrome, the chest pain usually is: Substernal Severe Lasts 30 mins! Dull, pressing, squeezing, tight, and cannot be localized by pointing to it by a finger, rather present in the substernal area. radiates to the arms and neck. precipitated by physical work (exercise, movement etc) and relieved by rest. could be associated with breathlessness, nausea, and vomiting, sweating, cough, hemoptysis, palpitations, dizziness, loss of consciousness; but these are not specific (sweating usually is). Acute coronary syndrome Is defined as myocardial ischemia due to myocardial infarction (NSTEMI or STEMI) or unstable angina. Testing for ACS AHA Guidlines: Any patient with Ischemic type pain should have an EKG done within 10 minutes of arrival. This is to be handed directly to the physician Causes of Myocardial Ischemia Either decreased oxygen supply (due to decreased perfusion; atherosclerosis, spasm, cocaine) or increased oxygen demand (hypertension, exercise, etc.) that can’t be met by the normal blood supply. Pathophysiology of the MI: Plaque rupture, and subsequent thrombus formation. If occlusive thrombus then STEMI. If non-occlusive, or unstable plaque then NSTEMI, or unstable angina. Vasospasm, such as seen in Prinzmetal’s angina or cocaine use. Progression of obstructive coronary atherosclerotic disease. If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the blocked coronary artery die (infarction), chiefly through necrosis, and do not grow back. A collagen scar forms in their place. When an artery is blocked, cells lack oxygen, needed to produce ATP in mitochondria. ATP is required for the maintenance of electrolyte balance, particularly through the Na/K ATPase. This leads to an ischemic cascade of intracellular changes, necrosis and apoptosis of affected cells. Cells swell up due to sodium and water following it. Lysosomes intracellular rupture and release their enzymes, digesting away the myocardial cells. That’s why time is essential, to prevent more damage! Cells in the area with the worst blood supply, just below the inner surface of the heart (endocardium), are most susceptible to damage. Ischemia first affects this region, the subendocardial region, and tissue begins to die within 15–30 minutes of loss of blood supply. The dead tissue is surrounded by a zone of potentially reversible ischemia that progresses to become a full-thickness transmural infarct.The initial "wave" of 26 infarction can take place over 3–4 hours. These changes are seen on gross pathology and cannot be predicted by the presence or absence of Q waves on an ECG. The position, size and extent of an infarct depends on the affected artery, totality of the blockage, duration of the blockage, the presence of collateral blood vessels, oxygen demand, and success of interventional procedures. Tissue death and myocardial scarring alter the normal conduction pathways of the heart, and weaken affected areas. The size and location puts a person at risk of abnormal heart rhythms (arrhythmias) or heart block, aneurysm of the heart ventricles, inflammation of the heart wall following infarction, and rupture of the heart wall that can have catastrophic consequences. Diagnosis Clinical symptoms Chest pain Heart failure Circulatory shock Electrocardiography ST segment abnormalities STEMI: ST elevated (>1mm) in 2 limb leads OR >2mm in 2 or more contiguous chest leads. You must start therapy; give thrombolytics (tPA if within less than 12 hrs) and do angioplasty. NSTEMI or Ischemia (causing the angina): ST depressed and T-wave inverted (don’t give thrombolytics, just monitor and you may start other treatment.) Laboratory parameters cTroponin Remains elevated for longer time than CK-MBin the blood after infarction Troponin I and T are cardiac specific (ath. Not AMI specific). Troponin T is abnormally elevated if > 15 ng/L 50% elevation of Tropnin T between measures done 3 hours apart are very indicative of acute ischemia. Elevates in 6 hrs Peaks in 12 h Remain elevated for 7 to 10 days (Elevates sooner and stays elevated longer) Higher specificity than CK-MB Not AMI specific, and can also be elevated in the case of heart failure, arrythmias, pulmonary embolism, kidney failure, severe hypertension and ACS. CK-MB Starts to elevate 6-8 hrs after the onset of ischemia Peaks at around 12-24 hours, and normalizes in 3-4 days Very good predictor of early reinfarction as it runs in cycles every 6-12 hours. There can be other conditions that elevate CK-MB such as heart muscle pathologies. 27 Myoglobin Not very sensitive, released by other organs Starts to rise the earliest. Abnormal in 80 – 100% AMI pts Small protein in striated and cardiac muscle, released in cell disruption Rises within 3 hours Peak at 4 to 9 hours Baseline at 24 hours Other lab markers: GOT LDH type 1 BNP: good in case of dysnpea due to cardiac problems other than AMI. hs CRP Echocardiography Quick analysis of the heart contractile function, e.g. if there is a localized contraction defect. Can also show valve function, pericardial fluid and a strained right ventricle in the case of pulmonary embolism. It has a high negative predictive value for ACS. 28 Reperfusion therapy STEMI Reperfusion therapy is indicated within 12 hours from the beginning of chest pain. Reperfusion can be done with thrombolysis and PCI. Ambulance control may alert the ED in advance of a patient with cardiac-type chest pain. Work efficiently as a team to ensure treatment is not delayed. Give O2 to maintain SpO 2 94–98% and attach cardiac monitor. Obtain IV access and take samples for U&E (urea and electrolytes), glucose, FBC, cardiac markers. Provide small increments of IV opioid analgesia titrated to effect. Ensure the patient has had 300mg aspirin and 300mg clopidogrel PO. Contact cardiology for primary percutaneous coronary intervention (PCI). Arrange transport to the cath lab. For patients undergoing PCI, consider IV glycoprotein IIb/IIIa receptor antagonist as an adjuvant. Be guided by local protocol. If PCI is not available, consider thrombolysis and monitor carefully. Start LMWH, heparin, or fondaparinux, according to local protocols. If pain continues, give IV GTN (glycerin trinitrate) (start at 0.6mg/hr and as necessary), provided systolic BP is >90mmHg. Consider beta blockers e.g. atenolol (5mg slowly IV over 5min, repeated once after 15min), or metoprolol, unless contraindicated (e.g. uncontrolled heart failure, hypotension, bradyarrhythmias, COPD). (Repeated)Indications for PCI or thrombolysis ST elevation of >1mm in 2 limb leads, or ST elevation of >2mm in 2 or more contiguous chest leads, or LBBB in the presence of a typical history of acute MI (NB: LBBB does not have to be new). Primary angioplasty for STEMI Primary percutaneous coronary intervention (coronary angioplasty and stenting) is the treatment of choice for STEMI. Compared with thrombolysis, PCI administered within 12hr of symptom onset results in lower mortality and re-infarction rates. The sooner it is performed, the greater the benefits. Thrombolysis If PCI cannot be performed within 90min of diagnosis, thrombolytic therapy is an alternative. The benefits reduce markedly with time delay, so if PCI is not available, do not delay the administration of a thrombolytic agent. Rural areas with long hospital transfers may have a protocol for ambulance administered thrombolysis, aided by telemedicine advice from the ED or cardiology. Patients presenting >12hr after symptom onset will not benefit from thrombolysis. Side Effects: Strokes, intracranial hemorrhage and major bleeds are more common in patients given thrombolysis. Intracranial bleeding is more common in older patients, those with hypertension on admission and those given tPA. Prior to administering thrombolysis, always explain the benefits and risks to the patient. Obtain verbal consent to give the 29 medication and record this in the notes. Contraindications to thrombolysis Head injury, recent stroke, previous neurosurgery or cerebral tumour. Recent GI or GU bleeding, menstruation, or coagulopathy/warfarin. Severe hypertension (eg systolic BP >200mmHg, diastolic BP>120mmHg), aortic dissection or pericarditis. Puncture of non-compressible vessel (e.g. subclavian vein), traumatic CPR, d GCS post- arrest. Major surgery within recent weeks. Pregnancy Choice of thrombolytic agents: Tissue plasminogen activator (tPA), rather than streptokinase, is the agent of choice. Always use tPA if streptokinase was given >5 days ago or in anterior MI in a patient 5 years). If already taking maintenance steroids, give 2mg/kg (max 60mg). In children who vomit, repeat the dose of prednisolone and consider IV hydrocortisone 4mg/kg. Add ipratropium bromide 0.25mg every 20–30 min if there is poor initial response to nebulized B-agonist. Consider salbutamol (15mcg/kg) given IV over 10min in severe cases with a poor response to initial nebulized salbutamol and ipratropium bromide. Refer to PICU urgently and check K + levels. Aminophylline is not recommended in children with mild to moderate asthma. In severe or life-threatening asthma unresponsive to maximal doses of bronchodilators and systemic steroids, take specialist advice and consider IV aminophylline (5mg/kg over 20min; maintenance IV infusion at 1mg/kg/hr; omit loading dose if already receiving oral theo-phyllines). Note: If possible, repeat and record peak flow 15–30min after starting treatment. If the patient is not improving, give further nebulized B-agonist. Pulse oximetry is helpful in assessing response to treatment. An SpO2 ≤92% in air after initial bronchodilator therapy usually indicates the need for more intensive in-patient care usually in PICU. CXR is indicated for severe dyspnea, focal chest signs, or signs of severe infection. Management of acute asthma in children aged 1 year. Perform abdominal thrusts from behind the child, placing your fist between the umbilicus and xiphisternum, and grasping it with your other hand, then pulling sharply inwards and upwards—repeat up to 5 times. Following chest or abdominal thrusts, if the object has not been expelled and the victim is still conscious then repeat the sequence of back blows and chest (for infant) or abdominal (for children) thrusts. Do not use abdominal thrusts for infants! If unconscious from foreign body airway obstruction If a child with foreign body airway obstruction is or becomes unconscious, place him on a flat surface, then open the mouth and look for any obvious object. If one is seen, use a single finger sweep to remove it. It may be possible to remove the FB with Magill’s forceps under direct laryngoscopy. Do not attempt blind or repeated finger sweeps. Open the airway and attempt 5 rescue breaths. If a breath does not make the chest rise, reposition the head before making the next attempt. If there is no response whilst attempting the 5 rescue breaths, proceed to chest compression with ventilation using a ratio of 15:2. Each time the airway is opened, check for a foreign body and if visible, try to remove it. If it appears that the obstruction has been relieved, open and check the airway. If the child is not breathing, deliver rescue breaths. If initial measures prove 39 unsuccessful and the child is hypoxic, oxygenate via a surgical airway until senior help arrives. Perform needle cricothyroidotomy in children aged 3 cm and sometimes a „show“; a mucus-blood discharge. There may be rupture of membranes. Stages of labour First: onset of labour until cervix is fully dilated (10 cm). Usually lasts > 6 hours. The upper part of the uterus contracts, the lower part, including the cervix dilates. Contractions increase in frequency (every 2 min) and duration (last 1 min). The head starts to descend. Second: full dilation until the baby is born. Lasts approx. 40 min in primigravida and 20 min in multigravida. Contractions of the upper part of the uterus, abdominal muscles and diaphragm cause head to descend and then rotate (usually to lie occiput anterior). An overwhelming desire to push helps expel the baby. Third: placenta and membranes deliver and uterus retracts (approx. 15 min). Assessment of patient in labour Check pulse, BP and palpate the abdomen. Listen for fetal heart sounds with fetal stethoscope or Doppler probe (rate should be 120-160/min). Gently examine the perineum. Do not fully examine the vagina unless the head is crowning and birth is imminent. Instead, transfer to the labour ward. Management of delivery Call obstetric/pediatric/anaesthetic help Offer 50:50 mixture of nitrous oxide and O2. Don sterile gloves and stand on the patients right. As head crowns discourage bearing down: advise rapid shallow breaths. Use left hand to control escape of the head (to prevent perineal tearing) Press gently forwards with right thumb and fingers either side of anus. Once head is delivered, allow it to extend. Feel for cord around neck: slip it over head, or if impossible, clamp and divide. Allow anteriour shoulder to deliver first (mother pushing if necessary) Give 5U oxytocin and 500 mcg ergometrine IM Deliver the baby, wrap the baby up and resuscitate as necessary. Management of the cord Once the baby cries and cord pulsation ceases, hold baby level with mother and clamp the cord twice (15 cm from umbilicus). Divide between clamps. Place a plastic Hollister crushing clamp 40 1-2 cm from umbilicus and cut 1 cm distally. Check that 2 normal arteries are present in the cord. Management of the third stage A few minutes after delivery, regular contractions begin again, causing the placenta to detach. The cord may be seen to move down accompanied by a small gush of blood. The placenta may be felt in the vagina. The Brandt-Andrews technique helps removal: apply gentle downwards traction on the cord whilst exerting upward pressure on uterus (preventing inversion). Examine the placenta carefully. Give Rhesus anti-D immunoglobulin if Rh neg. 41 Complications MOTHER Perineal tear: if a tear is imminent, perform an episiotomy because extensive tear risks the integrity of the external anal sphincter. Infiltrate 5-10 ml of 1% lidocaine postero-laterally from the posterior fourchette. Cut the perineal tissues postero-laterally using straight scissors with blunt points, avoiding large veins. After delivery, carefully examine the episiotomy wound which needs to be closed in layers using absorbable sutures. Uterine rupture When the muscular wall of the uterus tears during pregnancy or delivery. Risk factors include vaginal birth after c-section, uterine scars, obstructed labor, induction of labor and trauma. Diagnosis may be suspected based on a rapid drop in fetal HR during labour. Treatment involves rapid surgery to control the bleeding and deliver the baby. Hemorrhage Postpartum hemorrhage (PPH) is probably on if the most common obstetric emergencies. It can be: Primary: loss of > 500 mL blood from the genital tract within 24 h of delivery Secondary: loss of > 500 mL blood from the genital tract between 24 h and 12 w post delivery. Blood loss of 500-1000 mL are usually tolerated well by the woman, so it has been suggested that blood loss > 1000 mL should trigger emergency PPH protocols. The causes of PPH can be remembered as the 4T’s Tone = uterine atony Tissue = retained placenta and/or membranes Trauma = injury to vagina, perineum and uterine tears at c-section Thrombin = clotting disorders ATH! The earliest symptom of blood loss is usually tachycardia and BP often does not fall until massive haemorrhage has occurred (1200-1500 mL). Key points: Summon senior help Resuscitate Replace and maintain fluid volume Investigate status and cause of bleeding Arrest blood loss BABY Shoulder dystocia After delivery if the head, should dystocia occurs due to the shoulders being unable to pass under the maternal symphysis pubis. It results in excessive morbidity for both mother and fetus. There is risk of fetal hypoxia, death and fetal trauma in the form of fractures, usually long bones of arm or clavicle or brachial plexus injury. For the mother there is increased risk of bleeding and perineal trauma. Diagnosis is usually obvious when shoulders fail to deliver during next contraction after delivery of the head. Help should be summoned. The vessels of the fetal neck are occluded after the delivery of the head, and cerebral damage will occur if delivery is delayed. 42 Specific maneuvers are used to try to reduce the ant-post diameter of the shoulders and gain the maximum space in the maternal pelvis, including: Flexing and abducting the legs on the mother at the hips to flatten the lumbosacral spine (McRobert’s position) If that fails à apply suprapubic pressure If that fails à specific internal maneuvers PLACENTA AND CORD Cord prolapse Cord prolapse is the presence of the cord below the presenting part when the membranes are ruptured. It is diagnosed most commonly by seeing the cord at the introitus, or feeling it during a vaginal exam. Abnormal fetal HR pattern may suggest it as well, as compression of the umbilical vein between the presenting part and the pelvis, reduces or stops the flow of oxygenated blood to the fetus, causing deep variable decelerations, then bradycardia if the situation is not reversed. Immediate management aims to minimize the pressure of the fetal presenting part on the cord while plans are made to deliver the baby. This is achieved by moving the woman on to all fours with the head down, applying pressure vaginally to push the presenting part out of the pelvis, or by filling the bladder with 500 mL saline. There should be minimal handling of the cord as it can provoke spasms, worsening blood flow. Emergency c-section is required unless the cervix is fully dilated and assisted vaginal delivery can be performed. Placental abruption The separation of a normally sited placenta from the uterine wall. In most cases it is revealed as vaginal bleeding but it may be concealed and present as uterine pain and potential maternal shock or fetal distress without obvious bleeding. The fetus is at risk because of hypoxia following placental separation and premature delivery. The mother is at risk of hypovolemic shock, clotting disorders and consequent more widespread organ damage. The patient should be initially resuscitated using the structured approach of ABC. Uterine atony is the loss of tone in the uterine musculature. Normally, contraction of the uterine muscles during labor compresses the blood vessels and reduces flow, thereby increasing the likelihood of coagulation and preventing hemorrhage. A lack of uterine muscle contraction however can lead to an acute hemorrhage as the uterine blood vessels are not sufficiently compressed. Clinically, 75-80% of postpartum hemorrhages are due to uterine atony. Many factors can contribute to the loss of uterine tone including: overdistention of the uterus, multiple gestations, polyhydramnios, fetal macrosomia, prolonged labor etc. Management of uterine atony The first step is uterine massage. The next step is pharmacological therapies, the first of which is oxytocin, because it initiates rhythmic contractions of the uterus, compressing the spiral arteries which should reduce bleeding. In the first instance this would be a further bolus of the drug used to manage 3rd stage of labour and an infusion of oxytocin (40IU in 500 mL saline over 4 hours).The next step is the use of methylergometrine. It should not be used in those women with hypertension or pre-eclampsia. 43 The bladder should be catheterized as an empty bladder aids uterine contraction. Malpresentations Breech presentation Complications of breech labour include: increased risk of prolapsed cord, which can cause rapid hypoxia. Mechanical difficulties with the delivery of the shoulders and/or after-coming head: damage to visceral organs or brachial plexus. Poor progress in breech labour Is taken by most to be an indication for c-section. Limb presentation Extra info – from the lecture Initial assessment of the baby after birth: Term gestation? Breathing or crying? Good muscle tone? If 3 “yes” à baby can stay with mother If not à further medical care Airway, breathing: place baby under heat source, open airways in a neutral position, suction if needed (mouth then nose), dry the baby, reopen airway, skin stimulation. 44  Heart rate: auscultate for 6 sec. If < 100/min à pos. pressure ventilation, if cyanosis consider CPAP Chest compressions: after 30 sec ventilation if HR < 60/min. 3:1 ratio, 120/min of 90 compressions and 30 ventilations. iv. Lines: umbilical catheters, intraosseus, umbilical vein, ET is the last option Epinephrine: 0.01-0.03 mg/kg in every 3-5 min if after 30 sec effective ventilation plus 30-45 sec chest compression HR is still < 60/min. Fluids: if suspected hypovolemia, dose: 10-20 ml/kg. The first time and during CPR, in every 30 sec, reassess: breathing, HR and oxygenization (pulse oxymetry) 45  A. Surgical emergencies: acute appendicitis, acute pancreatitis, duodenal ulcer, peptic ulcer disease, perforation B. Airway management (airway opening maneuvers, equipment, indications and contraindications of NIV) Acute appendicitis This common cause of abdominal pain in all ages is particularly difficult to diagnose in the extremes of age and in pregnancy. However, the diagnosis of acute appendicitis is often missed initially at all ages. History The classic presentation is of CENTRAL colicky abdominal pain, followed by vomiting, then SHIFT of the pain to the right iliac fossa. Many presentations are atypical, with a variety of other symptoms (e.g. altered bowel habit, urinary frequency) partly depending upon the position of the tip of the inflamed appendix (retrocaecal 74%; pelvic 21%; paracaecal 2%; other 3%). Examination In the early stages, there may be little abnormal; in the late stages the patient may be moribund (at stages of death) with septic shock and generalized peritonitis. Between these extremes, there may be a variety of findings, including increased T°, tachycardia, distress, foetor oris (halitosis). There is usually a degree of tenderness in the right iliac fossa (±peritonitis). Rovsing’s sign (pain felt in the right iliac fossa on pressing over the left iliac fossa) may be present. PR examination may reveal tenderness high up on the right with inflammation of a pelvic appendix. Hamburger sign: anorexia (when asked, patient does not want to have his favourite food, a hamburger obviously) McBurnley point tenderness Rovsing‘s sign: deep palpation of LLQ causes RLQ referred pain Psoas sign: RLQ pain with extension of the right leg against resistance Obturator sign: RLQ pain with flexion and internal rotation of the right leg Investigations The diagnosis of acute appendicitis is essentially clinical. CT and X-rays are not routinely indicated, but perform urinalysis ± pregnancy test. Although FBC may reveal an increased WCC(white cell count), this is not invariable. Abdominal ultrasound may be helpful showing noncompressible and enlarged appendix. Differential diagnosis Depending upon the presentation, the potential differential diagnosis is very wide— remember to consider urinary, chest, and gynaecological causes. Treatment Obtain IV access and resuscitate if necessary. Commence IV fluids if there is evidence of dehydration. Give IV opioid and antiemetic (e.g slow IV metoclopramide 10mg). 46  If acute appendicitis is likely, or even possible, keep „nil by mouth“ (Nothing by mouth is a medical instruction meaning to withhold food and fluids from a person) and refer to the surgeon. If appendicectomy is required, pre-operative antibiotics (e.g cefuroxime + metronidazole) decreases risk of infective complications. Appendix mass Untreated, acute appendicitis may proceed to perforation with generalized peritonitis, or may become ‘walled off’ to produce a localized right iliac fossa inflammatory mass. There are many causes of such a mass. Refer to the surgeon for further investigation and management. Acute pancreatitis This is a relatively common serious cause of abdominal pain in the middle aged and elderly, with an incidence of ≈5 per 100,000/year. Causes Often due to gallstones and alcohol. Many are idiopathic. Other causes: hypothermia, trauma, infection (glandular fever, mumps, coxsackie, and infectious hepatitis), hyperlipidemia, hyperparathyroidism, drugs (steroids, azathioprine, thiazides, and statins), polyarteritis nodosa, pancreatic cancer. Symptoms Typically, the complaint is of severe constant epigastric pain radiating to the center of the back, with associated nausea and vomiting. 47 Signs The patient may be distressed, sweating and mildly pyrexial. Look for evidence of shock— there may be a need for urgent resuscitation. Abdominal tenderness is likely to be maximal in the epigastrium ± guarding. The often quoted, but uncommon bluish discoloration in the loins (Grey Turner’s sign) only develops after several days. Another sign is Cullen‘s sign, discoloration around the umbilicus. Other signs that can occur are pleural effusion, jaundice and ascites. Investigations Check blood glucose and SpO2 Serum amylase is likely to be grossly increased to >5 × upper limit of normal range (but if not diagnostically increased, consider urinary amylase level). FBC may reveal increased WCC. U&E, Ca 2+, LFTs, glucose—hypocalcaemia is relatively common. Coagulation screen. (pancreatitis causes hypercoagulability) CXR, ECG, ABG; consider lactate if unwell. Ranson score Treatment Provide oxygen. Obtain IV access and resuscitate with IV fluids as necessary. Give IV analgesia (e.g. morphine titrated according to response). Give an anti-emetic (e.g. cyclizine 50mg or metoclopramide 10mg slow IV). 48  Insert a nasogastric (NG) tube. Insert a urinary catheter and monitor urine output. Consider early insertion of a central venous line to monitor the central venous pressure (CVP) and guide IV fluid therapy in the seriously ill, particularly the elderly. Contact the appropriate specialist(s) and transfer to HDU/ICU. Complications of acute pancreatitis Acute pancreatitis has a significant mortality. Early complications include: acute renal failure (due to shock, prerenal failure. Could be postrenal if there was a thrombosis) disseminated intravascular coagulation (DIC) hypocalcaemia due to consumption of the calcium by fat necrosis. acute respiratory distress syndrome (ARDS). Later, pancreatic abscess or pseudo-cyst may occur. Chronic pancreatitis The term chronic pancreatitis implies permanent pancreatic damage. The condition often results from alcohol excess. Some patients with chronic pancreatitis present frequently to the ED requesting opioid analgesia. This can pose a difficult problem for the doctor who has not treated them previously so requesting previous hospital case notes early can be helpful. Peptic ulcer disease Perforated peptic ulcer History Perforation of a gastric or duodenal ulcer is usually a severely painful sudden event. It may occur in those without known peptic ulcer disease, as well as those with previously diagnosed problems. However, close questioning may reveal recent symptoms attributed to „indigestion“. Sudden localized epigastric pain spreads to the remainder of the abdomen— the pain is worse on coughing or moving and may radiate to the shoulder tip. Examination Although distressed, the patient often prefers to lie still, rather than roll about. However, some patients in extreme pain writhe or roll in agony and are unable to keep still for examination or X-rays until analgesia is given. Absent bowel sounds, shock, generalized peritonitis and fever develop as time passes. Investigations An erect CXR will demonstrate free gas under the diaphragm in ≈75% of patients with perforated peptic ulceration (if the patient is not fit enough for an erect CXR, obtain a left lateral decubitus X-ray). In those cases where the diagnosis is suspected, but not proven by X-ray, a contrast CT scan may help. Other relevant investigations are: U&E(urine and electrolytes test), glucose, amylase (may be slightly increased), FBC (WCC 49 typically increased), SpO2 , ABG, ECG/troponin (ensure symptoms do not reflect MI rather than peptic ulcer disease). Treatment Give O2. Provide IV analgesia (e.g. morphine titrated according to response). Give an antiemetic (e.g. slow IV metoclopramide 10mg). Resuscitate with IV 0.9% saline. Refer to the surgeon and give IV antibiotics (e.g. cefotaxime 1g and in late presentations, metronidazole 500mg as well). Other GI perforations Perforations may affect any part of the GI tract, but the chief causes are peptic ulceration, trauma, diverticular disease, and colonic carcinoma. The emergency treatment principles are similar to those of perforated peptic ulcer (described above). Bowel perforation usually results in gas under the diaphragm on an erect CXR, but remember that there are other possible causes including: recent surgery, peritoneal dialysis and gas-forming infections. Other presentations of peptic ulcer disease In addition to perforation; peptic ulcer disease may also present with upper or lower GI hemorrhage, or pain from esophagitis, gastritis or duodenitis. If the patient’s presentation suggests inflammation of the upper GI tract, consider discharging the patient with a supply of antacid and GP follow-up. This course of action is not appropriate if there is any possibility of serious complication. Similarly, it is not usually appropriate to initiate therapy with H2 blockers or proton pump inhibitors in the ED without an accurate diagnosis. 7B. Airway management (airway opening maneuvers, equipment, indications and contraindications of NIV) Airway opening maneuvers Chin lift – head tilt Jaw thrust: the key is to hook the little finger underneath the angle of the jaw. Use the ring and middle fingers to secure further grip under the mandible and the index finger and thumb can be used to help secure a tight seal between face and a mask for ventilation. The chin-lift is suitable for those patients who, with open airway are breathing adequately. The jaw thrust is more suitable for patients who require a bag-mask ventilation. Since movement of the head and neck is contrainicated in the suspicion of cervical spine injury use a jaw thrust. 50 Simple airway adjuncts Oropharyngeal and nasopharyngeal airways are designed to address airway obstruction. Oropharyngeal airway The correct size oropharyngeal airway should reach from the patients incisors to the angle of the jaw. Insertion method 1. Insert curved side up, twisting it 180° once inserted halfway. 2. The front end should sit just in front of the teeth. 3. Confirm that an improvement in ventilation has been achieved. Nasopharyngeal airway The key advantage of the nasopharyngeal airway is in those patient whose mouths are difficult to open, typically patients undergoing a seizure. Avoid using it in patients with obvious, significant mid-face injury. The internal diameter is stamped on the side of the tube. A 6 mm for women and 7 mm for men is recommended. Insertion method: 1. Lubricate the tube and instert into nostril aiming gently towards the occiput, curved side down. 2. Check for bleeding in oropharynx 3. Check for improvement in airway patency Oropharyngeal airway Nasopharyngeal airway Laryngeal mask airway Is a type of supraglottic airway device. It is composed of an airway tube that connects to an elliptical mask with a cuff which is inserted through the patients mouth, down the larynx and forms an airtight seal on the top of the glottis allowing a secure airway. 51 Tracheal tube A catheter inserted into the trachea to maintain a patent airway. There are different tracheal tubes: endotracheal tube, tracheostomy tube, tracheal button. Endotracheal tube: most of them have an inflatable cuff to seal the trachea and the bronchial tree against air leakage and aspiration of gastric contents, blood, secretions and other fluids. After having secured a patent airway, ask yourself if the patient needs: Ventilation Assisted ventilation An O2 mask Bag valve mask (ambu bag) A hand held device commonly used to provide positive pressure ventilation to patients who are not breathing or not breathing adequatly. 1. Mask to seal over patients face 2. Filter and valve to prevent backflow into the bag itself 3. The bag, squeezed to expel air to the patient. Bag and valve combinations can be attached to fx. ET tube or laryngeal masks instead of the mask. It can be connected to an oxygen source, delivering approx. 100% oxygen to the patient. In order to be effective the bag valve mask must deliver between 500-800 mL to the patients lungs. If supplemental oxygen is provided 400 mL might be adequate. Respiratory rate should be approx. 10-12/min (20/min for child/infant) 52 Non-rebreather mask Used to assist in the delivery of oxygen therapy. It requires the patient to be able to breath unassisted. Indications and contraindications for NIV (copied from google, don’t know how reliable) Noninvasive ventilation (NIV) is commonly ordered, and in many cases allows an opportunity for a patient to recover in lieu of intubation and mechanical ventilation. According to the National Institute of Health, the following are the indications: Acute respiratory failure Acute or chronic respiratory insufficiency Documented sleep apnea However nice NIV is, there are times when it is contraindicated. It is up to the respiratory therapists to remind the attending physicians of these contraindications when they arise. Contraindications for NIV are Absence of a drive to breathe Inability to maintain a patent airway Inability to adequately clear secretions Acute sinusitis or otitis media Risk for aspiration of gastric contents Hypotension (NIV may decrease cardiac output, decrease venous return) Pre-existing pneumothroax or pneumomediastinum Epistaxis Recent facial, oral or skull surgery or trauma History of allergy or sensitivity to mask materials where the risk from allergic reaction outweighs the benefit of ventilatory assistance. 53  A. Surgical emergencies: peritonitis, acute cholecystitis, ileus B. Bronchial asthma (pathomechanism, types, clinical features, treatment) Peritonitis: Acute peritonitis, or inflammation of the visceral and parietal peritoneum, is most often but not always infectious in origin, resulting from perforation of a hollow viscus (singular of viscera). This is called secondary peritonitis, as opposed to primary or spontaneous peritonitis, when a specific intraabdominal source cannot be identified. In either instance, the inflammation can be localized or diffuse. Clinical features: The cardinal signs and symptoms of peritonitis are acute, typically severe, abdominal pain with tenderness and fever. How the patient’s complaints of pain are manifested depends diffuse or localized. Elderly and immunosuppressed patients may not respond as aggressively to the irritation. Diffuse, generalized peritonitis is most often recognized as diffuse abdominal tenderness with local guarding, rigidity, and other evidence of parietal peritoneal irritation. Bowel sounds are usually absent to hypoactive. Most patients present with tachycardia and signs of volume depletion with hypotension. Laboratory testing typically reveals a significant leukocytosis, and patients may be severely acidotic. Radiographic studies may show dilatation of the bowel and associated bowel wall edema. Free air, or other evidence of leakage, requires attention and could represent a surgical emergency. In stable patients in whom ascites is present, diagnostic paracentesis is indicated, where the fluid is tested for protein and lactate dehydrogenase and the cell count is measured. Etiology Primary: Over 90% of the cases of primary or spontaneous bacterial peritonitis occur in patients with ascites or hypoproteinemia (40% have been reported for the elderly or immunocompromised. Successful treatment depends on correcting any electrolyte abnormalities, restoration of fluid volume and stabilization of the cardiovascular system, appropriate antibiotic therapy, and surgical correction of any underlying abnormalities. Secondary: Infective organisms may contaminate the peritoneal cavity after spillage from a hollow viscus, because of a penetrating wound of the abdominal wall, or because of the introduction of a foreign object like a peritoneal dialysis catheter or port that becomes infected. Secondary peritonitis most commonly results from perforation of the appendix, colonic diverticuli, or the stomach and duodenum. It may also occur as a complication of bowel infarction or incarceration, cancer, inflammatory bowel disease, and intestinal obstruction or volvulus. 54 Acute Cholecystitis: Impaction of gallstones with acute inflammation of the gallbladder usually manifests itself by right hypochondrial pain radiating to the right side of the back ± vomiting. Examination Look for features of an acute inflammatory process. Fever is frequently present, combined with right hypochondrial tenderness (particularly felt on inspiration—Murphy’s sign). There may be a palpable mass—this is also a feature of mucocele and empyema (the latter causing high fever, extreme tenderness and septic shock). Management Provide IV analgesia and anti-emetic Check FBC (WCC often increased), U&E, glucose, amylase, LFTs. CXR, ECG (in case pain is due to atypical presentation of MI). USS will confirm the diagnosis (tenderness on pressing the USS transducer over the area where the thickened gallbladder containing stones is located is called the ultrasonic Murphy’s sign). Commence antibiotics (e.g. cefotaxime 1g IV) and refer to the surgeon. Ileus Bowel obstruction is the interruption of the normal passage of bowel contents either due to a functional decrease in peristalsis or mechanical obstruction. Paralytic ileus is a temporary disturbance of peristalsis in the absence of mechanical obstruction. Postoperative ileus is the most common cause of paralytic ileus, which can also be caused by metabolic disturbances (e.g. hypokalemia), endocrinopathies (e.g. hypothyroidism) and certain drugs (e.g. anticholinergics). Mechanical bowel obstruction is classified according to location; either small bowel obstruction (SBO) or large bowel obstruction (LBO). The most common cause of SBO is postop. bowel adhesions, while the most common cause of LBO is malignant tumors. Regardless of cause, bowel obstruction typically manifests with nausea, vomiting, abdominal pain and distention, along with constipation or obstipation. Diagnosis Lab o If recurrent vomiting: § Hyperchloremic hypokalemic metabolic acidosis § Hyponatremia o If bowel strangulation § Metabolic acidosis § Hyperkalemia o Neutrophilic leukocytosis o If dehydration: increased Htc o If sepsis: abnormal coagulation profile o Potentially prerenal azotemia 55  Imaging o Abdominal series: erect and supine abdominal x-rays and erect chest x-ray. o Best initial test in unstable patients o Findings: dilation of bowel loops proximal to obstruction, minimal air within the bowel loops distal to the obstruction o 3-6-9 rule § Small bowel dilation if > 3 cm § Large bowel dilation if > 6 cm § Cecal dilation if > 9 cm o CT abdomen and pelvis is the best initial test in stable patients § With iv and/or oral contrast § Can help us see ischemia, perforation o MRI, US, barium enema Treatment Conservative: for partial bowel obstruction cases or complete cases with no signs of ischemia or necrosis. Fluid resuscitation, correction of electrolyte imbalace Intestinal decompression: NG tube insertion Bowel rest (NPO) IV analgesics and antiemetics Gradual increase of oral intake when pain and distention subside and bowel sounds return to normal Etiology-specific treatments Fecal impaction à washout Sigmoid volvulus à sigmoidoscopic detorsion Surgery If hemodynamically unstable or septic Complete obstruction with signs of ischemia/necrosis Persistant partial obstruction (>3-5 days) Closed loop obstruction Procedure: exploratory laparotomy Bowel rest The patient may be allowed sips of clear fluids, if tolerated. Once abdominal distention resolves and bowel sounds return, the patient can be started on a liquid diet. When the patient has taken adequate fluids, the diet can be advanced and intravenous fluid discontinued. 56 Bowel decompression (Decompression of the upper gastrointestinal tract is initiated early in the management to avoid vomiting, and to reduce gastric and small bowel distension.) For patients with moderate to severe or continuous vomiting, or significant abdominal distention, a nasogastric tube can be placed. Nutritional support Patients with postoperative ileus who are unable to tolerate enteral nutritional support will require total parenteral nutrition. Total parenteral nutrition (TPN) is a method of feeding that bypasses the gastrointestinal tract. Fluids are given into a vein to provide most of the nutrients the body needs. The method is used when a person cannot or should not receive feedings or fluids by mouth until they can be transitioned to oral feedings. Serial abdominal examination The abdominal examination should be evaluated several times per day to evaluate the amount of distention and patient discomfort. Repeated or more detailed imaging studies may be needed if ileus cannot be differentiated from bowel obstruction, or if conservative measures do not improve the patient's condition in 48 to 72 hours. 8B. Bronchial asthma (pathomechanism, types, clinical features, treatment) Asthma is a chronic obstructive condition, resulting from chronic inflammation of the airways, especially the bronchi and bronchioles, which subsequently results in increased contractablility of the surrounding smooth muscle. This among other factors leads to bouts of narrowing of the airway and the classic symptoms of wheezing. Chronically the airways‘ smooth muscle may increase in size along with an increase in the number of mucus glands. Clinical classification 57 Asthma is clinically classified according to the frequency of symptoms, FEV1 and peak expiratory flow rate. It may also be classicied as atopic or non-atopic based on whether symptoms are precipitated by allergens (atopic) or not. Asthma exacerbation Classic symptoms include: dyspnea, wheezing and chest tightness. Signs: use of accessory muscles of respiration, paradoxical pulse may be present (weaker during inspiration, stronger during expiration), cyanosis may occur. Emergency care of asthma bronchiale Measure the peak expiratory flow rate and compare it against that expected. Patients with life-threatening asthma may be too dyspnoeic to do this. Make an initial assessment of the severity of acute asthma based upon a combination of clinical features, peak flow measurements and pulse oximetry. Moderate exacerbation of asthma Increasing symptoms. Peak flow 50-75% best or predicted. No features of acute severe asthma. Acute severe asthma Any one of: Inability to complete sentences in 1 breath. Respiratory rate ≥25/min. Heart rate >110/min. Peak flow 33-50% best or predicted Life-threatening asthma A patient with severe asthma with any one of: Cyanosis. Exhaustion, confusion, coma. Feeble respiratory effort. SpO2 240/min Absence of isoelectric baseline Macro-re-entrant atrial tachycardia. Atrial flutter is an ECG definition of a P-wave rate >240/min, and an absence of an isoelectric baseline between deflections (flutter waves). (keep in mind that the flutter waves are not always positive waves; they can be positive or negative, depending on the direction of the reentry circuit) It is caused by a re-entrant circuit over large areas of the right or left atrium. The circuit is not influenced by adenosine and the AV node block reveals the underlying rhythm (explaining the AVN block; due to the 61 high rate of signals the AVN could be in its refractory time and therefore cannot conduct the current, therefore very commonly you observe a 2:1 block. Interventions that increase the AVN blockade (AVN blocking drugs, carotid massage, adenosine) to 3 or 4:1, ie pronouncing the block even more, makes the diagnosis easier. Atrial flutter exacerbates heart failure symptoms and if incessant will worsen LV function. Emergency situations management: Give O2, insert an IV cannula, and follow the algorithm (next page). The compromised patient with shock, syncope, acute cardiac failure, or cardiac ischaemia should be treated with emergency electrical cardioversion. It is reasonable to give IV adenosine while arranging the cardioversion, as long as this does not delay the procedure. For stable patients consider Vagal stimulation: The most effective way is a Valsalva maneuver while supine or tilted head down. Instruct the patient to attempt to blow the plunger out of a 50mL bladder tip syringe. If unsuccessful, in the young patient, massage the carotid sinus for 15sec (1 side only), by gently rubbing in a circular action lateral to the upper border of the thyroid cartilage. Carotid sinus massage may be dangerous (especially if there is a carotid bruit or previous stroke/TIA). Adenosine: This temporarily blocks conduction through the AV node. It has a very short half-life (10–15sec). Adenosine can successfully terminate re-entrant tachycardias and may ‘unmask’ other conditions (e.g. atrial flutter) by temporarily producing a conduction block. It is contraindicated in 2° or 3° AV block, patients with WPW and asthmatics (bronchospasms can occur). The effects are blocked by theophylline and potentiated markedly (and dangerously) in the presence of dipyridamole, carbamazepine or in a denervated heart—seek advice. Warn the patient about transient flushing and chest discomfort. Give adenosine by fast bolus 6mg IV injection into an IV cannula in the antecubital fossa and flush with 0.9% saline while recording a rhythm strip. If unsuccessful, repeat with 12mg, then 12mg. If adenosine is contra-indicated, consider IV verapamil 2.5–5mg over 2min. Avoid verapamil in patients with cardiac failure, hypotension, concomitant B-blocker therapy, or WPW. Monitor ECG, if still no sinus rhythm, then most likely Atrial flutter. Extra explanation of management, by cardiologists: DC cardioversion effectively restores sinus rhythm, but AFL often recurs. Drug therapy is not very effective. AVN blockade is difficult to achieve and the high doses of beta blockers, calcium channel blockers and digoxin may have unwanted side effects. 62  Class 1C drugs are used to maintain SR however, 1: AV node blockers propafenone and flecainide can paradoxically accelerate the ventricular rate in AFL by slowing the tachycardia rate down sufficiently to allow the AVN to conduct 1:1. Therefore they should be always used in combination with an AVN blocking agent. (beta blockers, calcium channel blockers, digoxin). Amiodarone is an alternative agent particularly if LV function is impaired. RFA (radio frequency ablation) is the most effective way of maintaining SR and is a cure. Refer to a cardiologist, can’t do this in an emergency clinic. Extra: in some cases, the RFA isn’t sufficient, and effective rate control isn’t possible with drugs, then ablation of the AV node and a pace maker is a permanent palliation solution. Note: Anticoagulation recommendations for pts. with AFL are identical to those for pts with AF. Atrial Tachycardia Management Algorithm 63 9B. Differential diagnosis of headache Patients typically present in one of three ways: Severe headache, unlike any previous one (‘first severe’ or ‘worst ever’) Headache with associated worrying features (altered mental status, fever, focal neurology). Chronic severe headache unresponsive to treatment. Causes Primary headaches Migraine. Tension headaches. Cluster headaches. Miscellaneous (benign cough headache, benign exertional headache, headache associated with sexual activity). Secondary headaches Head injury. Vascular (stroke, intracranial haematoma, subarachnoid haemorrhage, unruptured arterio-venous malformation, venous thrombosis, hypertension). Non-vascular intracranial disorder (increased CSF pressure, post-LP, intracranial tumour). Substance misuse or withdrawal. Infection (encephalitis or meningitis). Metabolic (hypoxia, hypercapnoea, hypoglycaemia, carbon monoxide poisoning, dialysis). Craniofacial disorders (pathology of skull, neck, eyes, nose, ears, sinuses, teeth, mouth, temporomandibular joint dysfunction). Neuralgias (trigeminal, occipital and other cranial nerves). Approach SAH (sudden, severe onset, syncope). Meningitis and encephalitis (fever, neck rigidity). Head injury (history or signs of trauma). Increased ICP (papilloedema, loss of retinal vein pulsation). Stroke (focal neurologic signs). Acute glaucoma (painful red eye, decreased visual acuity (VA), irregular semi-dilated pupil). Cranial arteritis (jaw pain, temporal artery tenderness). Examination Check GCS, pulse rate, respiratory rate, BP, T°, and SpO2. Feel the head for muscular tenderness, arterial tenderness, trigger points for neuralgia, and look for evidence of head injury. Examine the eyes for visual acuity, pupil reactions, and eye movements. Look at the fundi for papilloedema. Palpate the sinuses for tenderness. Look at the ears for haemotympanum or infection. 64  Check the oral cavity for infection. Look for evidence of purpura/rash of meningococcal infection. Complete a full neurological examination (including cranial nerves, limb tone, sensation, co-ordination and reflexes). Check for Kernig’s sign: straightening the knee whilst the hip is flexed produces discomfort in the presence of meningeal irritation. Management Check FBC, ESR, CRP, U&E, blood glucose. If pyrexial, take blood cultures and consider IV cefotaxime 2g. Start IV fluids and admit. An effective treatment for headache is IV metoclopramide 10mg with IV fluids. Emergency CT for any patient with an acute severe headache or with a history of seizure, or an abnormal neurological exam. Arrange a CT for any patient with HIV. If subarachnoid haemorrhage is suspected and CT normal, admit for lumbar puncture. 65  10.A. Shock (types, treatment, cardiogenic and hemorrhagic shock) B. Mushroom poisoning (types, treatment, Amanita phalloides poisoning Shock is a state of severe systemic reduction in tissue perfusion characterized by decreased cellular O2 delivery and utilization as well as decreased removal of waste byproducts of metabolism. Recognized by: Hypotension: Systolic BP 100/min) is common, but may not be present in patients with cardiac or neurologic causes or in those taking β- blockers. Altered consciousness and/or fainting may result from decreased cerebral perfusion. Poor peripheral perfusion: Cool peripheries, clammy/sweaty skin, pallor, decreased capillary venous return, but note that in the early phase of endotoxic septic shock there may be vasodilation with warm peripheries. Oliguria: Decreased renal perfusion with urine output 24 hours) nephrotoxic à cortinarius rhabdomyolysis à tricholoma Investigations Should be guided by clinical assessment Check LFTs and renal function first if GI symptoms present > 6 hours after exposure Consider: FBC, U&E, crea, coagulation, CK, glucose, ECG, ABG and lactate Mycologist examination of mushroom samples. Management Resuscitation rarely necessary life-threats include: § gastroenteritis and hypovolemic shock § seizures and coma § cholinergic crisis Supportive care and monitoring Decontamination activated charcoal 50g (1g/kg in children) if onset of GI symptoms occurs > 6 hours post-ingestion. Antidotes cyclopeptide hepatotoxicity (amatoxins) § N-acetylcysteine § Penicillin § Silibinin 70  Cholinergic syndrome § Atropine Seizures § pyridoxine Amanita phalloides poisoning causes vomiting and profuse watery diarrhoea after a latent period of 6-12 hrs, followed by hepatic and renal failure. The interval between ingestion and the onset of symptoms is crucial in distinguishing between non-serious and potentially fatal poisoning. Symptoms Initially, symptoms are gastrointestinal in nature and include colicky abdominal pain, with watery diarrhea and vomiting, which may lead to dehydration, and, in severe cases, hypotension, tachycardia, hypoglycemia, and acid–base disturbances. These first symptoms resolve two to three days after the ingestion. A more serious deterioration signifying liver involvement may then occur—jaundice, diarrhea, delirium, seizures, and coma due to fulminant hepatic failure and attendant hepatic encephalopathy caused by the accumulation of normally liver-removed substance in the blood. Renal failure (either secondary to severe hepatitis or caused by direct toxic renal damage) and coagulopathy may appear during this stage. Life-threatening complications include increased intracranial pressure, intracranial hemorrhage, pancreatitis, acute renal failure, and cardiac arrest. Death generally occurs six to sixteen days after the poisoning. 71  11.A. Acute coronary syndrome (clinical features and treatment) B. Hypothermia (causes, pathomechanism, clinical features, treatment) Acute coronary syndrome is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly and dies. The most common symptoms include chest pain (often radiating to the left shoulder, or the angle of the mandible) and can be associated with nausea and sweating. It is commonly associated with those clinical manifestation: Unstable angina: angina at rest, new onset exertional angina, recent acceleration of angina or post revascularization angina. NSTEMI STEMI (Sudden cardiac death) It is of important to note that women often describe chest pain differently to men and might not be as decisive when describing their symptoms. Sometimes dyspnoea, fatigue and palpitations are the main complains and then it is described as angina equivalent. Diagnosis: Clinical symptoms Chest pain Heart failure Circulatory shock ECG ST segment abnormalities Elevation = 1 mm, but 2 mm in V1-3 Depression = horizontal, ascending, descending Acute LBBB Lab parameters cTroponin CK Other: myoglobin, GOT, LDH, BNP, hs CRP Echocardiography Has high negative predictive value Reperfusion therapy Indicated within 12 hours from the beginning of the chest pain. Thrombolysis PCI (percutaneous coronary intervention) 72 Absolute contraindications of thrombolysis History of hemorrhagic stroke History of stroke, dementia or CNS damage within 1 year. Head trauma or brain surgery within 6 months Known intracranial neoplasm Suspected aortic dissection Internal bleeding within 6 weeks. Active bleeding or known bleeding disorder Major surgery trauma or bleeding within 3 weeks Traumatic CPR within 3 weeks. Relative contraindications of thrombolysis Oral coagulation therapy Acute pancreatitis Pregnancy or within 1 week postpartum Active peptic ulceration TIA within 6 months Dementia Infective endocarditis Advanced liver disese Intracardiac thrombi Uncontrolled hypertension (>180/110) Puncture of non compressible blood vessel within 2 weeks 73 PCI uses medical equipment such as a guide wire, balloon catheters, stents. M-guard stent, a bare metal stent Drug eluding stent (DES) Drugs ASA: 75-325 mg/d to all patients unless contraindicated, then give Clopidogrel § Usually a loading dose of 300 mg po. on arrival. If pt. was already taking it, 75 mg. Na-Heparin/LMWH § 5000 IU +/I Clopidogrel (based on possibility of CABG) § Double anti-platelet therapy for 9-12 months after ACS, longer if stented. Glycoprotein IIb/IIIa inhibitors (given in the cath lab) Beta blockers (especially in anterior wall infarct, use with caution in inferior infarcts) NTG (consider morphine if pain is not relieved, use with caution in inferior infarcts) ACE-I § Anti-remodelling after MI Statins Activate the cath lab! 11B. Hypothermia (causes, pathomechanism, clinical features, treatment) Hypothermia exists when the core temperature is 32°C); wrapping in warm blankets + polythene sheets. Endogenous metabolism and shivering usually generates enough heat to allow spontaneous rewarming. Active rewarming: A water bath (not recommended) at ~41°C is rapid and useful for immersion hypothermia but cannot be used in injured patients or if CPR is required. Hot water bottles and heat pads are less efficient and can cause burns. A hot air blanket is more convenient than a water bath, provides some heat and reduces heat loss. Core rewarming: Airway warming with heated (40-45°C) humidified O2 provides some additional heat and reduces heat loss. Peritoneal lavage: saline at 45°C. The fluid directly heats the liver and retroperitoneal structures including blood in the IVC. Warm IV fluids. Extracorporal rewarming with cardiopulmonary bypass maintains brain and organ perfusion and, if available, is the method of choice in patients with severe hypothermia or cardiac arrest 76 12. A. Junctional tachycardias (AVRT and AVNRT) B. Sepsis (pathomechanism, clinical features, treatment) Junctional tachycardias (AVRT, AVNRT) They are supraventricular tachycardias (SVTs) characterized by the involvement of the AV node (increased automaticity in or near the AV node). Can be classified based on site of origin (atria or AV node) or regularity (regular or irregular). Can be seen in digitalis toxicity. Classification based on QRS width is unhelpful as this is also influenced by the presence of pre-existing bundle branch block, rate-related aberrant conduction or presence of accessory pathways. ECG features Junctional rhythms are arbitrarily classified by their rate: Junctional Escape Rhythm: 40-60 bpm Accelerated Junctional Rhythm: 60-100 bpm Junctional Tachycardia: > 100 bpm Narrow complex rhythm; QRS duration < 120ms (unless pre-existing bundle branch block or rate-related aberrant conduction). Ventricular rate usually 60 – 100 bpm. Retrograde P waves may be present and can appear before, during or after the QRS complex. Retrograde P waves are usually inverted in the inferior leads (II, III, aVF), upright in aVR + V1. AV dissociation may be present with the ventricular rate usually greater than the atrial rate. 77 AVNRT (AV Nodal Reentry Tachycardia) Regular rhythm, rate 150 – 250/min P waves occur during or after QRS Narrow QRS complex This is the commonest cause of palpitations in patients with structurally normal hearts. AVNRT is typically paroxysmal and may occur spontaneously or upon provocation with exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines). It is more common in women than men (~ 75% of cases occurring in women) and may occur in young and healthy patients as well as those suffering chronic heart disease. Patients will typically complain of the sudden onset of rapid, regular palpitations. The patient may experience a brief fall in blood pressure causing presyncope or occasionally syncope. If the patient has underlying coronary artery disease the patient may experience chest pain similar to angina (tight band around the chest radiating to left arm or left jaw). The patient may complain of shortness of breath, anxiety and occasionally polyuria due to elevated atrial pressure releasing atrial natriuretic peptide. The tachycardia typically ranges between 140-280 bpm and is regular in nature. It may cease spontaneously (and abruptly) or continue indefinitely until medical treatment is sought. The condition is generally well tolerated and is rarely life threatening in patients with pre- existing heart disease. In comparison to AVRT, which involves an anatomical re-entry circuit (Bundle of Kent), in AVNRT there is a functional re-entry circuit within the AV node. Functional pathways within the AV node In AVNRT, there are two pathways within the AV node: The slow pathway (alpha): a slowly-conducting pathway with a short refractory period. The fast pathway (beta): a rapidly-conducting pathway with a long refractory period. During sinus rhythm, electrical impulses travel down both pathways simultaneously. The impulse transmitted down the fast pathway enters the distal end of the slow pathway and the two impulses cancel each other out. However, if a premature atrial contraction arrives while the fast pathway is still refractory, the electrical impulse will be directed solely down the slow pathway (1). By the time the premature impulse reaches the end of the slow pathway, the fast pathway is no longer refractory (2) — hence the impulse is permitted to recycle retrogradely up the fast pathway. This creates a circus movement whereby the impulse continually cycles around the two pathways, activating the Bundle of His anterogradely and the atria retrogradely (3). The short cycle length is responsible for the rapid heart rate. This is the most common type of re-entrant circuit and is termed Slow-Fast AVNRT. Similar mechanisms exist for the other types of AVNRT. 78 General features of AVNRT Regular tachycardia ~140-280 bpm. QRS complexes usually narrow (< 120 ms) unless pre-existing bundle branch block,