Emergency Medicine (Quesmed) Flashcards
What are the 5 pathogenic causes and 3 other causes of Acute Epiglottitis?
Haemophilus influenzae b (Hib)
Streptococcus spp
Staphylococcus aureus
Pseudonomas
Herpes Simplex
Thermal Causes
Foreign Bodies
Radiotherapy Related Inflammation
What are the 5 signs of Acute Epiglottitis and what should be done in these patients?
Fever
Drooling
Stridor
Pain
Children would prefer to sit upright
These patient should not be examined, treated or cannulated but left alone as any upset or distress may lead to total airway obstruction
What is the 3 step management of Acute Epiglottitis?
An urgent referral to ENT and anaesthetics should be made urgently
After their airway had been secured, patients need to urgently intubated and ventilation and treatment should be provided
Depending on the cause, oral and IV antibiotics should be started
What are the causes of Acute Pancreatitis?
GET SMASHED
Gallstones (most common cause worldwide)
Ethanol (most common cause in Europe)
Trauma
Steroids
Mumps
Autoimmune diseases (Polyarteritis Nodosa/ SLE)
Scorpion fight
Hypercalcaemia, Hypertriglycerideamia, Hypothermia
ERCP
Drugs
What are the drug causes of Acute Pancreatitis?
FAT SHEEP
Furosemide
Azathioprine/ Asparaginase
Thiazides/ Tetracycline
Statins/ Sulfonamides/ Sodium Valproate
Hydrochlorothiazide
Estrogens
Ethanol
Protease Inhibitors and NRTIs
Thiazides, Furosemide, some HIV drugs (protease inhibitors and non-nucleoside reverse transcriptase inhibitors), Sulfasalazine and Gliclizide are classed as Sulfonamides
What are the 9 signs of Acute Pancreatitis?
-A Stabbing, Epigastric Pain which radiates to the Back and is relieved by sitting forward or laying in the foetal position
- Vomiting
- A Recent Alcohol Binge or a Recent History of Gallstones suggests Acute Pancreatitis
- Hypovolaemia (Tachycardia, Dry Mucosal Membranes due to Third-space Loss of Fluids)
- Fever is only present if the Pancreatitis has been complicated with Infection
- Haemorrhagic Pancreatitis is rare but there may be Grey-Turner’s Sign which is Bruising along the Flanks
- There may be Guarding in the Epigastric Region but this is a Non-Specific Sign
- Cullen’s Sign is bruising around the Peri-Umbilical Region
- Third-space Fluid Sequestration in Pancreatitis is the result of a Combination of Inflammatory Mediators, Vasoactive Mediators and Tissues which leads to Vascular Injury, Vasoconstriction and Increased Capillary Permeability- this leads to Extravasation of Fluid into the Third Space
(This can lead to Acute Respiratory Distress Syndrome, Pleural Effusions and Hypovolaemia which leads to Acute Kidney Injury)
What are the 5 Blood Tests should be ordered if Acute Pancreatitis is suspected?
FBC (Leukocytosis can indicates Necrotising Pancreatitis)
Urea and Electrolytes
LFTs may be abnormal in Gallstone Disease
Lipase is a more sensitive and specific marker than Amylase and should be used over Amylase
An Amylase level is 3 times the upper limit of normal, this suggests Acute Pancreatitis
What 3 conditions can also elevated Amylase in addition to Acute Pancreatitis?
A Perforated Duodenal Ulcer
Cholecystitis
Mesenteric Infarction
What are the 4 Imaging Investigations that should be ordered if Acute Pancreatitis is suspected?
Ultrasound Abdomen can look for Gallstones
MRCP can be used to look for Obstructive Pancreatitis
ERCP is preferred generally over MRCP
A CT Scan can be performed at a later stage if Complications of Pancreatitis are suspected- such as Pseudocysts or Necrotising Pancreatitis
What Glasgow Criteria Score suggests transfer to ITU in Acute Pancreatitis and how long after admission should this score be worked out?
A score above 3 suggests admission to ITU and this should be worked out 48 hours after admission
What is the Glasgow Criteria Score criteria?
PANCREAS
PaO2<8kPa
Age>55 years old
Neutrophils- WBC>15x10^9/L
Calcium<2mmol/L
Renal Function- Urea>16mmol/L
Enzymes- AST/ALT>200ui/L or LDH>600ui/L
Albumin<32g/L
Sugar- Glucose>10mmol/L
What is the 7 step management for Acute Pancreatitis?
(Maintain electrolyte imbalances and compensate for third space losses)
- Aggressive Fluid Resuscitation with Crystalloids
(Aim to keep urine output>30mL/hour)
Start with a 1 litre bolus and try to maintain adequate urine output. This usually amounts to a fluid requirement of 3-5ml/kg/hour - Catheterisation
- Analgesia (strong analgesia in the form of Opioids is needed)
- Anti-emetics
- IV Antibiotics are shown to have No Real Effect in Outcome unless Necrotising Pancreatitis is present. Necrotising Pancreatitis is a complication of Severe Pancreatitis representing inadequate fluid resuscitation in initial management. This is usually diagnosed through a CT scan. Routinely giving antibiotics in Acute Pancreatitis is not in current clinical practice
- Calcium may be given if Hypocalcaemia is present but this is not prescribed prophylactically
- Insulin may also be given if there is Hyperglycaemia due to the damaged pancreas not being able to release the hormone
What is Pulseless Electrical Activity and Asystole?
These are both Non-Shockable Rhythms (Use CPR Instead)
Pulseless Electrical Activity is where the ECG shows that a pulse should occur but you do not actually feel a pulse in the patient
Asystole is a Cardiac Arrest Rhythm with no discernible Electrical Activity on the ECG Monitor
What is the management of Pulseless Electrical Activity and Asystole?
CPR should be commenced immediately
Adrenaline 1mg IV should be given in the first cycle and if the rhythm continues, then give Adrenaline every other cycle (1st, 3rd, 5th etc)
What is Ventricular Fibrillation and Pulseless Ventricular Tachycardia?
These are both Shockable Rhythms
Ventricular Tachycardia is a regular broad complex tachycardia
Ventricular Fibrillation presents as chaotic irregular deflections of varying amplitude
What is the management of Ventricular Fibrillation and Pulseless Ventricular Tachycardia?
Defibrillation and CPR should be conducted
However, if the rhythms persist, Amiodarone 300mg IV and Adrenaline 1mg IV can be given after the Third Shock
Amiodarone is given as a One-Off Dose but Adrenaline can be repeated every other cycle (3rd, 5th, 7th etc)
What are the 7 causes of Airway Compromise?
Angioedema
Anaphylaxis
Thermal Injury
Neck Haematoma
Wheeze
Surgical Emphysema
Reduced Consciousness
What are 3 simple Airway Maneouvres?
Suction- if there is visible vomit, blood or foreign bodies in the Airway
(Turn patient onto their side if they are actively vomiting, unless they have a C-spine injury)
Head-tilt/ Chin lift- Aim for the Sniffing Position- can be achieved manually or by placing a pillow under the head
Jaw Thrust- Using both hands, hook your fingers under the angle of the patient’s jaw and move their mandible forward
What are 2 common Airway Adjuncts (ways to keep the airway open after manual manouevres) (3,2)
Oropharyngeal Airway-
- a Rigid Plastic Tube
- Measured from the Incisors to the Angle of the Jaw
- It is inserted upside down and then rotated 180 degrees to keep the tongue away from the Posterior Pharynx
Nasopharyngeal Airway-
- a Flexible Rubber Tube
- This passed through one of the Anterior Nasal Passages and sits Inferiorly at the Base of the Tongue
- This is typically used if the patients have a strong gag reflex to the Oropharyngeal Airway
- This is contraindicated if the patient has a Base of Skull Fracture
What is a Supraglottic Airway? (4)
They are Flexible Plastic Tubes with Inflatable Cuffs
They are devices which can be used with Ventilation Machines
Examples include the Laryngeal Mask Airway (LMA) or i-Gel
They sit over the Top of the Larynx
What is an Endotracheal Tube? (4)
It is a Flexible Plastic Tube with an Inflatable Cuff
It is inserted through a Laryngoscope and used for Prolonged Mechanical Ventilation
It protects the airways against Aspiration (Cuffed Endotracheal Tube with the Cuff Inflated below the Vocal Cords)
If this is not successful, you can insert a Supraglottic Airway such as an iGel or Laryngeal Mask Airway, or Bag-Valve Mask Ventilation
What are the 3 indications for Bag-Valve Mask Ventilation?
Respiratory Failure (Hypoxia or Hypercapnia) associated with a respiratory rate of less than 10
Apnoea
Cardiac Arrest
What are the 6 main signs of Opioid toxicity?
Poor Respiratory Rate/ Effort
Bilateral Pinpoint Pupils
Decreased Conscious Level
Multiple Needle/ Track Marks on Skin
Confusion
Cyanosis if severe
What 3 things should be identified in a patient presenting with Alcohol Withdrawal?
An Associated Health and Psycho-social problem
The severity of the alcohol misuse (AUDIT Questionnaire and SADQ Questionnaire)
Whether there is any risk to themselves or to others
What are the 7 presentation signs of a Simple Alcohol Withdrawal? (6-12 hours after the last drink)
Insomnia
Tremor
Anxiety
Agitation
Nausea and Vomiting
Sweating
Palpitation
What is the presentation of Alcohol Hallucinosis? (12-24 hours after last drink)
Visual, Tactile or Auditory Hallucinations
What are the 6 signs of Delirium Tremens?
Delusions
Confusion
Seizures
Tachycardia
Hypertension
Hyperthermia
What are the 7 indications for Inpatient Alcohol Withdrawal? (risk factors for them getting withdrawal while admitted)
Patients drinking >30 units of Alcohol per day
Scoring over 30 in the SADQ Score
High Risk of Alcohol Withdrawal Seizures (Previous Alcohol Withdrawal Seizures or Delirium Tremens or History of Epilepsy)
Simultaneous withdrawal from Benzodiazepines
Significant Medical or Psychiatric Comorbidity
Vulnerable Patients
Patients under 18 years old
What is the 4 step management for Alcohol Withdrawal?
(if drinking >15 units a day or >20 on the AUDIT Questionnaire)
Chlordiazepoxide prescribed in a reducing regimen according to the CIWA Score and Local Protocol
If they have Alcohol-Withdrawal Seizure, they should be prescribed a Rapid-Acting Benzodiazepine (like IV Lorazepam)
Pabrinex (1 pair of Ampoules a day to prevent Wernicke’s Encephalopathy)
- If there are signs of Wernicke’s Encephalopathy (Confusion, Ataxia, Ophthalmoplegia or Nystagmus), patients should be prescribed 2 pairs of Ampoules
In Delirium Tremens (Confusion and Visual Hallucinations 48-72 hours after Abstinence) give Oral Lorazepam first line. If symptoms still continue, then give Parenteral Lorazepam.
What are the 6 Gastrointestinal causes of Central Abdominal Pain and 3 Non-Gastrointestinal causes?
Gastrointestinal causes-
- Bowel Obstruction
- Early Appendicitis
- Acute Gastritis
- Acute Pancreatitis
- Ruptured Abdominal Aortic Aneurysm
- Ischaemic Bowel Disease
Non-Gastrointestinal causes-
- Pneumonia
- Acute Coronary Syndrome
- Diabetic Ketoacidosis
What are the 6 Clinical Features of Ascending Cholangitis?
Charcot’s Triad- but only occurs in a Third of Patients
(Right Upper Quadrant Pain, Fever, Jaundice)
Hypotension, Tachycardia and Confusion if the Sepsis is severe
What are the 3 causes of Ascending Cholangitis?
Biliary Calculi (stones)- 50% of cases
Benign Biliary Stricture
Malignancy
What 5 investigations should be ordered if Ascending Cholangitis is suspected?
Bloods- Raised LFTs and Raised Inflammatory Markers (WCCs and CRP)
Ultrasound Abdomen- to detect Bile Duct Dilatation- not good at picking up stones in the mid/distal area of the Biliary Duct
CT Scan- gives good detail of the Biliary Tree and can show Radiopaque Stones (although the most common stones are actually Radiolucent Stones)
MRCP is the most accurate imaging method and can view almost all causes of Biliary Tree Blockage
Once the cause is determined, use ERCP to Intervene
What is the 6 step management for Ascending Cholangitis?
Resuscitation (Intravenous Fluids and Antibiotics)- The patient may require Critical Care based on the Severity of Shock and Organ Failure
Biliary Drainage may be required
Endoscopic Drainage- ERCP (Endoscopic Retrograde Cholangiopancreatography)- stent placement for strictures
Percutaneous Drainage- PTC (Percutaneous Transhepatic Cholangiography)
Surgical Drainage
Assessment and management of Predisposing Cause- Like Cholecystectomy for Gallstones
What is the management of a Conscious Choking Adult? (4)
Encourage the patient to cough
Give them 5 back blows with the heel of the palm aiming between the shoulder blades
Give them 5 abdominal thrusts performed from behind the patient with a fist placed between the umbilicus and the xiphisternum, grasping it upwards and pulling upwards and inwards sharply
Continue these motions until the obstruction is dislodged or the patient becomes unconscious
What is the management of an unconscious choking patient?
Call for help and start ABC
Airway-
- Open the mouth and observe if the obstruction is visible and removable. Only attempt to remove an object if under direct vision
- Open the airway with a jaw thrust or head tilt/ chin lift
Breathing-
- If the patient is not breathing, start cardiopulmonary resuscitation
What are the 5 signs of Benzodiazepine toxicity?
Lethargy
Ataxia
Slurred Speech
Coma
Respiratory Distress
What are the 4 signs of Beta-Blocker toxicity?
Bradycardia
Hypotension
Mild Hypoglycaemia
Mild Hyperkalaemia
What are the 5 signs of Cyanide toxicity?
Nausea and Vomiting (if small doses)
Rapid Loss of Consciousness
Apnoea
Seizures
Cardiac Arrest
What are the 5 signs of Phenothiazine (Chlorpromazine) toxicity?
Dystonia
Sedation
Dry Mouth
Hyperthermia
Dysrhythmias
What are the 7 signs of Organophosphate toxicity?
Salivation
Lacrimation
Urination
Diarrhoea
Small pupils
Fasciculations
Bradycardia
What are the 6 signs of MDMA (Ecstasy) toxicity?
Agitation
Tachycardia
Hypo/ Hypertension
Hyperthermia
Acute Renal Failure
Mydriasis
What is Compartment Syndrome?
It is where Muscle Swelling and Inflammation leads to an Increase in Pressure in the Muscle Compartment
This is a Limb Threatening Condition as the increase in Pressure causes a Loss of Blood Supply to that limb and Ischaemia
What are the 5 signs of Compartment Syndrome?
Severe Pain (specifically in the Passive Flexion of the Toes)
Pallor
Paralysis of the Limb
Pulselessness
Paresthesia
What is the treatment of Compartment Syndrome (3)?
Urgent Fasciotomy
Analgesia
Fluids
What is Deep Vein Thrombosis?
The Intra-luminal Occlusion of any Vein that is within the Deep System of a Limb (either the arm or leg) or the Pelvis
What are the 11 risk factors for Deep Vein Thrombosis?
Age>60
Active Cancer
Dehydration
Recent Orthopaedic or Pelvis Surgery
Long-distance Travel
Obesity
Previous history of Venous Thromboembolism
Family history of Venous Thromboembolism
Thrombophilias
Combined Oral Contraceptives and Hormone Replacement Therapy
Pregnancy
What are the 4 signs of Deep Vein Thrombosis?
Unilateral warm, Swollen Thigh or Calf
Pain on Palpation of Deep Veins
Distension of Superficial Veins
Pitting Oedema
What 3 investigations should be ordered if Deep Vein Thrombosis is suspected?
D-dimer-
- Used when there is a low probability of DVT
- It is Highly Sensitive but not Specific so it can Only EXCLUDE DVT but not Confirm it
- Other things may raise D-Dimer such as (6) Malignancies, Pregnancies, Strokes, Myocardial Infarctions, Infections and Aortic Dissections
Doppler Ultrasound-
- This is the Investigation of Choice
- Do this if there is a high probability of a DVT
- It is not the Gold-Standard as DVTs can be missed if the image quality is suboptimal
Digital Subtraction or CT/MR Venogram-
- All three can be used to evaluate the extent of the DVT and look for rare underlying causes such as May-Thurner Syndrome
- Digital Subtraction Venography is the Gold-Standard but is rarely used as it is Highly Invasive
What is the 4 step management of Deep Vein Thrombosis?
Anticoagulation- either a Direct Oral Anticoagulant (DOAC), Low Molecular Weight Heparin (LMWH) or Warfarin (which can be bridged with LMWH). NICE Guidelines recommend a DOAC like Apixaban or Rivaroxaban as First-Line Therapy.
- Duration is at least 3 Months
- Patients with Active Cancer should be Anticoagulated for at least 3-6 Months
- Patients with Unprovoked DVTs should be considered for Anticoagulation for over 3 Months (Typically 6 Months)
- Those with Recurrent DVTs should be considered for Life-long Therapy
Percutaneous Mechanical Thrombectomy-
- Used in Massive DVTS
IVC Filter-
- This will not treat the DVT itself but will reduce the risk of the DVT embolising into the pulmonary arteries and causing a Pulmonary Embolism
- This is used in patients where Anticoagulation is Contraindicated
Further Investigations-
- Consider an investigation of Occult Malignancy if there are other Relevant Symptoms
- Consider a Thrombophilia Screening if this is clinically relevant
What are the 4 complications of a Deep Vein Thrombosis?
Pulmonary Embolism
Venous Insufficiency
Recurrent Deep Vein Thrombosis
Post-Thrombotic Syndrome- Pain, Swelling, Hyperpigmentation, Dermatitis, Ulcers, Gangrene and Lipodermatosclerosis= caused by Chronic Venous Hypertension
What is Disseminated Intravascular Coagulation (DIC)
This is the inappropriate activation of the clotting cascades which results in Thrombus Formation and Depletion of Clotting Factors and Platelets
What are the 7 signs of Disseminated Intravascular Coagulation (DIC)?
Excess Bleeding (Epistaxis, Gingival Bleeding, Haematuria, Bleeding from Cannula Sites)
Fever
Confusion
Coma
Petechiae (small pinpoint red/pink spots)
Brushing
Hypotension
What are the 5 risk factors of Disseminated Intravascular Coagulation (DIC)?
Major Trauma/ Burns
Multiple-Organ Failure
Severe Sepsis or Infection
Severe Obstetric Complications
Solid Tumours or Haematological Malignancies
What is the subtype of Acute Myeloid Leukaemia that is associated with Disseminated Intravascular Coagulation?
Acute Promyelocytic Leukaemia
What are the 4 investigation findings of Disseminated Intravascular Coagulation?
Thrombocytopaenia
Increased Prothrombin Time
Increased Fibrin Degradation Products (such as D-Dimer)
Decreased Fibrinogen
What 3 signs point to Moderate Asthma Exacerbation and what 4 signs point to Severe Asthma Exacerbation?
Moderate Asthma Exacerbation-
- Increasing Symptoms
- PEF> 50-75%
- No features of Severe Asthma
Severe Asthma Exacerbation-
- PEF 33-50%
- Respiratory Rate is 25 or more
- Heart Rate is 110 or more
- They are unable to complete a sentence in one breath
What are the features of Life-Threatening Asthma? (33,92 CHEST)
These patients Must be Admitted
PEF<33%
SO2<92% or PO2<8
Cyanosis
Hypotension
Exhausted, Altered Consciousness
Silent Chest
Tachyarrhythmias
What should be remembered about patients with Life-Threatening Asthma and their PCO2 levels?
They may have normal PCO2 levels (4.6-6) as they are unable to ventilate properly (even though you would expect them to have Low PCO2 levels)
A Raised PCO2 is a sign for Near-Fatal Asthma
What are the 6 Criteria for referring Asthma Exacerbation Patients to Intensive Care?
2 things about resporation
2 things about o2 and co2
peak flow
and one more thing
If they require Ventilatory Support
If they have Severe or Life-Threatening Asthma who is failing to respond to therapy which is shown by (5)-
- Deteriorating Peak Flow Reading
- Persisting or Worsening Hypoxia
- Hypercapnia
- Exhaustion, Feeble Respiration
- Respiratory Arrest
What is the 4 step Immediate Management for an Asthma Exacerbation?
Sit up
100% O2 via a Non-Rebreathe Mask (aim for 94-98%)
Nebulised Salbutamol (5mg) and Ipratropium (0.5mg)
Hydrocortisone 100mg IV or Prednisolone 50mg PO
What should be added to the Immediate Management of an Asthma Exacerbation if the patient has Life-Threatening Asthma? (3)
Inform the Intensive Care Team
Magnesium Sulphate 2g IV over 20 minutes
Nebulised Salbutamol every 15 minutes
What should be done if there is no improvement in the Asthma Exacerbation following the Immediate Management? (4)
Nebulised Salbutamol every 15 minutes
Continue Ipratropium 0.5mg 4-6 hourly
Consider Aminophylline unless they are already on Theophylline
ITU Transfer for Invasive Ventilation
What 3 things should be done/ monitored in the Monitoring following an Asthma Exacerbation?
SpO2 should be kept above 92%
Take Peak Flow Measurements every 15-30 minutes pre- and post- Salbutamol
Take Consecutive Arterial Blood Gas measurements
What are Unstable Angina (3), NSTEMI (3) and STEMI(3)?
Unstable Angina (the narrowing of coronary arteries caused by Ischaemia)
- Chest pain at Rest or at Minimal Exertion which lasts>15 minutes
- ECG Changes (new ST Depression or T Wave Inversion)
- No Rise in Troponin (no Myocardial Necrosis)
NSTEMI (Partially Occluded Coronary Arteries)
- Chest pain at Rest or at Minimal Exertion which lasts>15 minutes
- ECG Changes (new ST Depression or T Wave Inversion)
- Rise in Troponin (Myocardial Necrosis)
NSTEMI and Unstable Angina are differentiated by the Rise in Troponin seen in NSTEMI
STEMI (Completely Occluded Coronary Artery)
- Chest pain at Rest or at Minimal Exertion which lasts>15 minutes
- ECG Changes (new ST Elevation or Left Bundle Branch Block)
- Rise in Troponin (Myocardial Necrosis)
NSTEMI and STEMI are differentiated by their ECG Changes
Chest pain may not ALWAYS be there
How is a STEMI diagnosed?
New ST-segment elevation in 2 or more contiguous leads (leads next to each other)
The ST Elevation should be more that 2mm in the Precordial Leads or more than 1mm in the limb leads
What is the management of a STEMI?
MMONAC
Morphine
Metoclopramide
Oxygen (if sats are less than 94%)
Nitrates (GTN Spray)
Aspirin 300mg
Clopidogrel 300 mg (Although drugs like Ticagrelor are sometimes used instead in practice)
If the patient is within 12 hours of symptom onset and within 2 hours of medical contact- then consider Percutaneous Coronary Intervention. They should be Haemodynamically stable.
If they present within 12 hours of symptom onset but after 2 hours of medical contact- then consider Thrombolysis if they are stable and there are no contraindications. If there are contraindications, then consider Percutaneous Coronary Intervention.
If they present more than 12 hours of symptom onset, Pharmacotherapy should be considered if they are Asymptomatic and Unstable. Otherwise, Revascularisation can be considered.
What are the 7 Contraindications to Thrombolysis in Myocardial Infarction?
Aortic Dissection
Gastrointestinal Bleeding
Allergic Reaction
Iatrogenic (Recent Surgery)
Neurological Disease (Recent Stroke (within 3 months), Malignancy)
Severe Hypertension (more than 200/120)
Trauma (including Recent CPR)
What is an NSTEMI?
It is a type of Acute Coronary Syndrome with typical Acute Coronary Syndrome signs, no ST segment elevation on the ECG and Raised Cardiac Biomarkers
What is the management of an NSTEMI?
MMONAC
Morphine
Metoclopramide
Oxygen (if sats<94%)
Nitrates (GTN Spray)
Aspirin 300mg
Clopidogrel 300mg
After MMONAC, stratify the patient according to either the Thrombolysis in Myocardial Infarction Score (TIMI Score) or the GRACE model depending on the hospital’s choice
If the Patient has a high risk of death and further ischaemic events should be offered re-vascularisation within 12-24 hours
If the Patient has a low risk of death- they can be managed conservatively with Medications
They can be discharged after having stabilised (once they don’t have symptoms and their cardiac biomarkers are normal) and they should have Further Cardiac Investigations in the Future
What is the 5 step Emergency Management of Chronic Obstructive Pulmonary Disorder (COPD)? (3 points for each category)
Oxygen Therapy
- Sit up
- Administer 24% Oxygen via Venturi mask: SpO2 88–92%
- Vary FiO2 and SpO2 target according to the Arterial Blood Gases
Nebulised Bronchodilators (Air Driven)
- Salbutamol 5mg/4h
- Ipratropium 0.5mg/6h
Steroids-
- Hydrocortisone 200mg IV
- Prednisolone 40mg PO for 7-14d
Antibiotics (if evidence of infection)
Further treatments if no response
- Repeat Nebulisers and consider Aminophylline IV
- Consider NIV (BiPAP) if pH<7.35 and/ or Respiratory Rate >30
- Consider Invasive Ventilation if pH<7.26
What is Acute-Angle Closure Glaucoma?
It occurs when a high intra-ocular pressure causes damage to the Optic Nerve
This occurs due to the Closure of the Iridio-corneal Angle in the eye
What are the 3 risk factors for Acute-Angle Closure Glaucoma?
Being Female, Being Asian, The use of certain medications such as those with Anti-muscarinic properties, such as Amitriptylline
What are the symptoms of Acute-Angle Closure Glaucoma (5)? What is seen in examination (3)?
Sudden Headache
Nausea
Red Eye
Symptoms worsen at night
Haloes when they look at Bright Lights
On Examination-
- Red Eye
- Cloudy Cornea
- Mid-dilated Pupil
What is the initial (3) and definitive management for Acute-Angle Closure Glaucoma?
Administering IV Acetazolamine and a Beta Blocker such as Timolol
Muscarinic Agonists such as Pilocarpine eye drops may be given
An urgent referral to Ophthalmology should be made
Definitive-
- Peripheral Iridotomy
What are the 5 complications of Acute-Angle Closure Glaucoma?
Temporary loss of vision
Malignant Glaucoma
Iris Sphincter Atrophy
Permanently dilated pupil
Permanent Blindness
What causes an Anaphylactic Shock?
Type 1 IgE-mediated Hypersensitivity which occurs when a patient is exposed to certain medications or food or bee stings.
Patients are often Hypotensive
What are the 5 signs of an Anaphylactic Shock?
Skin Reactions (Widespread Urticaria, Itching, Flushed Skin)
Respiratory Symptoms (Swollen Tongue/ Lips, Sneezing, Wheeze)
Gastrointestinal Symptoms (Abdominal Pain, Nausea, Vomiting, Diarrhoea)
Tachycardia
Hypotension
What confirms a diagnosis of Anaphylactic Shock?
Serum levels of Mast Cell Tryptase
What is the 8 step management for an Anaphylactic Shock? What is the 3 step management if the relevant skills and equipment are available?
Remove Trigger
Call for help early
ABCDE Assessment
Administer Oxygen
Lie Patient Flat and Raise Legs
Administer Adrenaline (500mg IM for Adults)
Administer Chlorphenamine and Hydrocortisone
IV Fluids should be given if they are Hypotensive
If skills and equipment are available-
- Manage airway
- Attach Patient to Monitoring
- Consider Intensive Care referral
What is Atrial Fibrillation?
Abnormal Electrical Impulses start firing in the atria. These pulses override the heart’s natural pacemaker
For Fast Atrial Fibrillation, the heart rate is over 100bpm
What are the 4 indications for DC Cardioversion in Atrial Fibrillation?
Shock
Syncope
Acute Pulmonary Oedema (does not include Chronic Heart Failure)
Myocardial Ischaemia
If there are no indications for DC Cardioversion, how should Atrial Fibrillation be managed?
Atrial Fibrillation with a duration of less than 48 hours can be safely cardioverted
If the duration is unknown or is more than 48 hours, Anticoagulation can be started at a minimum of 3 weeks before and 4 weeks after Cardioversion due to the risk of a Stroke from a Left Atrial Appendage Thrombus
If patients are not Cardioverted, they may need Life-long Anticoagulation based on their CHA2DS2 VaSc Score
When should Carbon Monoxide Poisoning be suspected in patients?
If they have had issues with their boiling or heating at home
What are the 5 signs of Carbon Monoxide Poisoning?
Confusion
Nausea and Vomiting
Cherry Red Skin
Tachycardia
100% Oxygen Saturation of Pulse Oximetry
What 4 investigations should be ordered if Carbon Monoxide Poisoning is suspected?
VBG/ ABG- A Carboxyhaemoglobin Concentration of over 20% is diagnostic
Chest Xray- Evidence of Acute Respiratory Distress Syndrome (Asymmetrical Consolidations)
ECG- Ischaemic Changes
Bloods- including Creatine Kinase (Rhabdomyolysis)
What is the 2 step management for Carbon Monoxide Poisoning?
100% Oxygen via Face Mask- helps unbind Carbon Monoxide from the Haemoglobin Molecule
Hyperbaric Oxygen- Controversial but it is the Gold Standard
What is Cardiac Tamponade?
It is the accumulation of blood in the Pericardial Sac
The volume and pressure of this blood can impact the cardiac filling
What is the main cause of Cardiac Tamponade?
Penetrating wounds- caused by road traffic accidents or pacemaker insertions
Other causes include (3)
- Pericarditis
- Malignancy
- Inflammatory Conditions- like SLE
What are the 4 signs of a Cardiac Tamponade?
Beck’s Triad- Raised JVP, Hypotension and Muffled Heart Sounds
Kussmaul’s Sign- JVP raises with Inspiration
Pulsus Paradoxus- A Drop in the Systolic Blood Pressure with Inspiration
An ECG may show Electrical Alternans (Alternating Height
What is the diagnostic investigation of choice for a Cardiac Tamponade?
An Echocardiogram
What is the management of a Cardiac Tamponade?
Pericardiocentesis
What characterises Diabetic Ketoacidosis (3)?
Hyperglycaemia (may not always be present)
(Blood glucose over 11mmol/L)
Acidosis (Bicarbonate below 15mmol/L or Venous pH less than 7.3)
Ketonaemia (3mmol/L and over)
What are the 4 main causes of Diabetic Ketoacidosis?
Infection (so they may have a Fever, which isn’t a symptom of DKA but of a potential cause of it)
Dehydration
Fasting
Presentation of Type 1 Diabetes
What are the 8 signs of Diabetic Ketoacidosis?
Smell of Acetone (Fruity Breath)
Vomiting
Dehydration
Abdominal Pain
Hyperventilation (Kussmaul/ Deep Sighing)
Hypovolaemic Shock
Drowsiness
Coma
What 7 investigations should be ordered if Diabetic Ketoacidosis is suspected?
Blood Glucose (>11.1 mmol/L)
Blood Ketones (>3mmol/L)
Urea and Electrolytes
Blood Gas Analysis
Urinary Glucose and Ketones
Blood Cultures (if evidence of Infection)
Cardiac Monitoring/ ECG- any Ischaemic changes or changes secondary to Hypokalaemia
What is the 3 step management of Diabetic Ketoacidosis?
If the patient is Alert, not significantly Dehydrated and able to Orally Intake without vomiting= Encourage Oral Intake and give a Subcutaneous Insulin Injection
If the patient is Vomiting, Confused or significantly Dehydrated= give IV Fluids (initial Bolus of 10ml/kg 0.9% NaCl then discuss with a senior) and Insulin Infusion at 0.1 units/kg/hour- 1 hour after starting IV Fluids. If there is evidence of a shock, the initial Bolus should be 20ml/kg
If the patient is Shocked or in Comatose- ABCDE Assessment should be carried out
Do NOT Stop the Intravenous Insulin Infusion until 1 hour after Subcutaneous Insulin Infusion had been given
What is the main complication of Diabetic Ketoacidosis? And what is the theory behind how it may occur?
Cerebral Oedema
It results from the rapid correction of dehydration with IV Fluids
This is why it is recommended fluid should be taken slowly over 48 hours
What is Ethylene Glycol Poisoning?
Ethylene Glycol is found in anti-freeze and can be ingested accidentally or intentionally
What are the 9 Early Features of Ethylene Glycol Poisoning (<24 hours)?
What are the 4 Late Features of Ethylene Glycol Poisoning? (>24 hours)
Early Features-
- Apparent intoxication (similar to that of Alcohol)
- Nausea and Vomiting
- Haematemesis
- Seizures
- Ataxia
- Ophthalmoplegia
- Papilloedema
- Raised Anion Gap Metabolic Acidosis
- Pulmonary Oedema
Late Features-
- Acute Tubular Necrosis
- Hypocalcaemia
- Hyperkalaemia
- Hypomagnesaemia
What is the 4 step management of Ethylene Glycol Poisoning?
Gastric Lavage or NG Aspiration if <1 hour since ingestion
Fomepizole (Competitive inhibitor of alcohol dehydrogenase)- prevents metabolism of Ethylene Glycol into toxic metabolites
Alcohol (Ethanol) can be used if Fomepizole is unavailable
Haemofiltration can be used in severe cases
What is an Extradural Haemorrhage?
It is a collection of blood between the inner surface of the skull and the outer layer of the dura. It is commonly caused by a Torn Middle Meningeal Artery
What are the 6 signs of an Extradural Haemorrhage?
Recent Head Injury
Headache
Nausea and Vomiting
An Altered Mental State
Sometimes Seizures
6th Nerve Palsy- This nerve has a long Intracranial Course so is susceptible to damage following Herniation secondary to an Increased Intracranial Pressure- this is known as a False Localising Sign
How is an Extradural Haemorrhage diagnosed?
CT Head- which shows a Bi-convex (Lentiform) shaped Haematoma which is Hyperdense
What is the 3 step management for an Extradural Haemorrhage?
Conservative Monitoring
Blood Pressure Reduction
Surgery (if Severe) like Burr Holes
What are the 4 causes of Hyperosmolar Hyperglycaemic State from Type 2 Diabetes?
Infection
Medications that cause Fluid Loss or Lower Glucose Tolerance
Surgery
Impaired Renal Function
What are the 7 signs of Hyperosmolar Hyperglycaemic State?
And 4 signs if they are extremely unwell?
Nausea and Vomiting
Lethargy
Weakness
Confusion
Dehydration
Coma
Seizure
4 signs of extreme unwellness
- Hypovolaemia
- Tachycardia
- Hypotension
- Exhaustion
What are the 3 investigations that suggest a diagnosis of a Hyperosmolar Hyperglycaemic State?
Severe Hyperglycaemia (30mmol/L or more) (not accompanied by Significant Acidosis (pH>7.3 or bicarbonate>15mmol/L) or Ketosis (ketones>3mmol/L))
Hypotension
Hyperosmolality (usually more than 320 mosmol/kg)
What is the difference between Diabetes Ketoacidosis and Hyperosmolar Hyperglycaemia State?
HHS and DKA, rather than being distinct entities are a spectrum of metabolic disturbance in diabetes.
The main difference is that the presence of endogenous insulin production in Type 2 diabetics is sufficient to ‘switch off’ ketone production and prevent diabetic ketoacidosis
What are the management principles for a Hyperosmolar Hyperglycaemic State?
Rehydration to correct the Hypotension and Electrolyte Abnormalities.
Correction of Hyperglycaemia- Partially Achieved through Fluid Therapy
What are Hyperosmolar Hyperglycaemic State patients at risk of?
Thrombosis due to Hyperviscosity so VTE Prophylaxis is an important part of management.
Remember Virchow’s Triad (Blood Stasis, Endothelial Injury, Hypercoagulability)- Hyperviscosity leads to Blood Stasis
What is the 3 step management of Hyperosmolar Hyperglycaemic State?
- Fluid Resuscitation with 0.9% Saline (1L over 1–2 hours, 1L (+KCl) over 2-4 hours,1L (+KCl) over 4-6 hours, 1L (+KCl) over 6-8 hours, 1L (+KCl) over 8-10 hours)
Change to 0.45% Saline if failing to reduce osmolality by 5mOsm/kg/hour
- Insulin at 0.05 units/kg/hour (only if ketones>1mmol/L or if Glucose fails to fall). Continue any Long Acting Insulin
- Venous Thromboembolism Prophylaxis
What is the Anion Gap? (2)
The formula (Na + K) - (Cl + HCO3)
The normal anion gap is 10-18 mmol/L
When there are lots of Acids in the blood, The H+ depletes the HCO3 in the equation so the anion gap Increases causing Metabolic Acidosis
What can cause Metabolic Acidosis?
The accumulation of Endogenous Acids (Lactic Acid, Ketones, Urate) or Exogenous Acids (Salicylates, Ethylene glycol, Methanol)
Paracetamol overdose can also cause metabolic acidosis in extreme cases
SALICYLATE poisoning can cause Respiratory Alkalosis at early stages due to the respiratory centres being stimulated and hyperventilation occurring as a result
What are the 3 signs of Pericarditis?
Sharp Pleuritic Chest Pain relieved by leaning forwards (they may have a had a Flu-Like Prodrome)
Pericardial Friction Rub (usually the Only Sign)
ECG- PR Depression and Saddle Shaped ST Elevation. Also slightly elevated Troponin levels
What is the 4 step management of Pericarditis?
Analgesia (NSAIDs like Aspirin or Ibuprofen)
Bed rest
Colchicine
Steroids
Also treat the underlying cause
What are the 2 main complications of Pericarditis?
Cardiac Tamponade
Chronic Constrictive Pericarditis
What 5 signs are seen in the Chest Examination of a Pneumothorax patient?
Reduced Chest Expansion on the affected side
Hyper-resonant Percussion on the affected side
Reduced or Absent Breath Sounds on the affected side, with no added sounds
Vocal Resonance (or Tactile Vocal Fremitus) is reduced on the affected side
Additional signs seen in a Tension Pneumothorax- signs of Haemodynamic Compromise (Tachycardia and Hypotension) and Tracheal Deviation to the Contralateral side
Which investigation should be ordered if a Pneumothorax is suspected?
Chest Xray
What is the 3 step management of a Tension Pneumothorax?
ABCDE algorithm. High flow Oxygen (15L/min) via a Non-rebreather Mask
Emergency management through Immediate Needle Decompression using a 16-gauge Cannula inserted at the Second Intercostal Space, Mid-Clavicular Line on the Affected Side
The needle should be inserted above the Third Rib to avoid damaging the Neurovascular Bundle. The needle decompression acts as a bridge before insertion of an Intercostal Chest Drain
What is the 2 step management of a Primary Pneumothorax?
If the patient is NOT Short of Breath AND the Pneumothorax is less than 2cm on Chest Xray they can be Discharged and reviewed in 2-4 weeks
If the patient IS Short of Breath OR the Pneumothorax is more than 2cm, the patient should be Aspirated with a 16-18 Gauge Cannula under Local Anaesthetic. If this is successful, the patient can be discharged. If not, an Intercostal Chest Drain is needed and the patient must be admitted
What is the 3 step management of a Secondary Pneumothorax?
If the patient is NOT Short of Breath AND the Pneumothorax is less than 1cm on the Chest Xray, they do not require further invasive intervention and should be admitted for Observation for 24 hours and Admitted Oxygen
If the patient is NOT Short of Breath AND the Pneumothorax is 1-2cm on the Chest Xray, they need to be Aspirated. If this is successful, they can be admitted for 24 hours of Observation. If this is Not Successful, Intercostal Chest Drain is necessary
If the patient IS Short of Breath OR the Pneumothorax is more than 2cm on the Chest Xray, an Intercostal Chest Drain is necessary and they should be Admitted
What are the 5 signs of a Pulmonary Embolism?
2 of these are Triads
Sudden onset of Shortness of Breath, Pleuritic Chest Pain and Haemoptysis (The Typical Triad although this is Rare)
If the Pulmonary Embolism is Massive, there will also be signs of Shock and Syncope
A Small Pulmonary Embolism may be Asymptomatic
Tachypnoea, Tachycardia and Hypoxia may be present. (Triad 2) There may be Low-grade Pyrexia and Tachycardia may be the only presenting symptom
A Massive Pulmonary Embolism may present with Hypotension, Cyanosis and signs of Right Heart Strain (Raised JVP, Parasternal Heave and loud P2)
What are the ECG Findings associated with Pulmonary Embolism?
May be normal or may have Sinus Tachycardia
If Massive Pulmonary Embolism, there may be evidence of Right Heart Strain (4) (P Pulmonale, Right Axis Deviation, Right Bundle Branch Block and nonspecific ST/T wave changes)
S1Q3T3 (deep S waves in lead 1, pathological Q waves in lead 3 and inverted T waves in lead 3) are very rare
What 6 blood tests should be ordered in Pulmonary Embolism?
Arterial Blood Gas- Type 1 Respiratory Failure, Hypoxia without Hypercapnia and/ or Respiratory Alkalosis (due to Hyperventilation occurring secondary to Hypoxia
FBC (patient may be Anaemic if they have Haemoptysis)
CRP may be raised
U&Es (to assess their Renal Function before CT Pulmonary Angiogram (CTPA))
Clotting Functions (important if the patient is to be started on LWMH or Warfarin)
D-Dimer- useful in Ruling out a Pulmonary Embolism but Not Confirming it
What 4 imaging investigations should be ordered in a Pulmonary Embolism?
Chest Xray- Typically Normal in a Pulmonary Embolism but you may see (3) Fleischner Sign (Enlarged Pulmonary Artery), Hampton’s Hump (Peripheral Wedge Shaped Opacity) and Westermark’s Sign (Regional Oligaemia). Chest Xray can rule out differentials such as Pneumonia and a Pneumothorax
CT Pulmonary Angiogram- Diagnostic Test of Choice- will show a Filling Defect in the Pulmonary Vasculature. If the Patient has (3) a Renal Impairment, Contrast Allergy or is Pregnant, a V/Q scan is preferred
Lower Limb Duplex- helpful if a Deep Vein Thrombosis (DVT) is thought to be the cause of the Pulmonary Embolism (this is First Line if the patient is Pregnant)
Bedside Echocardiogram- Used if the Patient has a Massive Pulmonary Embolism (signs of Right Heart Strain/ Hypotension) in order to assess their suitability for Thrombolysis
What should be ordered based on the Well’s Score in Pulmonary Embolism?
If the Well’s Score is 4 or less, the D-Dimer should be measured. The D-Dimer has a High Negative Predictive value but a Low Specificity so it is only useful if the Suspicion of Pulmonary Embolism is Low
A Low D-Dimer Excludes a Pulmonary Embolism. A Raised D-Dimer suggests that they should have Diagnostic Imaging such as CTPA/V/Q scan
If the Well’s Score is more than 4, further Diagnostic Investigations are needed. Low Molecular Weight Heparin is usually given if the suspicion of a Pulmonary Embolism is high and should be administered if there is a delay in performing a CTPA anyway
What is the Acute Management approach to a Pulmonary Embolism?
ABCDE + Alteplase if Massive
DR ABCDE
Airway- Likely to be patent (normal airway, like if the patient is talking)
Breathing- They may be Tachypnoeic and Hypoxic and Oxygen should be Administered
Circulation- They may be Tachycardic. Signs of Right Heart Strain suggest a Sub-Massive Pulmonary Embolism. Hypotension suggests a Massive Pulmonary Embolism. Consider IntraVenous Fluids if their Systolic Blood Pressure is less than 90mmHg
Disability- Likely to be Unremarkable
Exposure- They may have Low-Grade Pyrexia. Check for signs of Deep Vein Thrombosis. Consider Analgesia at this stage, if the patient requires it
If there are signs of a Massive Pulmonary Embolism, Thrombolysis (through an IntraVenous Bolus of Alteplase) is needed. There is debate as to whether this should be done in a Sub-Massive Pulmonary Embolism
What is the Medical Management approach to a Pulmonary Embolism? (6)
Anticoagulation should be administered
If in OutPatients, Direct Oral Anticoagulants like Apixaban or RIvaroxaban should be administered
If neither of the Above are suitable, Dabigatran, Edoxaban or Warfarin can be considered.
Low Molecular Weight Heparin should be continued for at least 5 days, until 48 hours of an INR lower than 2 has been achieved if they are on Warfarin. If they are on Dabigatran or Edoxaban, then Low Molecular Weight Heparin should be used for 5 days prior
The duration of anticoagulation treatment depends on the aetiology of the Pulmonary Embolism. A Provoked Pulmonary Embolism (where the cause can be identified such as Surgery or Pregnancy) should be treated for 3 months. Unprovoked Pulmonary Embolisms should be treated for Life
If a patient already on Warfarin has a Venous Thromboembolism (such as PE or DVT), the INR target should be increased 3 or 4
In the Inpatient/ Emergency Setting, Low Molecular Weight Heparin is used instead as it is Short-Acting
What is the Interventional Management of a Pulmonary Embolism?
An Embolectomy may be considered in patients with a Massive Pulmonary Embolism when Thrombolysis is Contraindicated
An Inferior Vena Cava Filter may be considered in patients with Recurrent DVTs on Warfarin, OR patients who can not have Anticoagulation
What is Status Epilepticus?
Any seizure activity that lasts more than 5 minutes or if they experience more than one seizure and does not fully regain consciousness between the two seizures
What is the 9 step management of Status Epilepticus?
ABCDE Approach
Oxygen
Ensure IV Access
Arterial Blood Gas
Take Bloods for (8) Glucose, FBC, U&Es, CRP, Calcium, Phosphate, Magnesium and Drug Levels if they are on Anti-epileptic Medication
Anaesthetic Review to ensure the Airway is managed
IV Lorazepam 4mg (a second dose should be given if there is no response) and if there is No IV Access, PR Diazepam or Buccal Midazolam should be given
If the initial Benzodiazepine fails, further Anticonvulsants can be used such as (3) Leviteracetam, Phenytoin, Valproate
If the Seizures continue to persist, Intubation and General Anaesthesia are needed
What is Supraventricular Tachycardia?
Any Narrow Complex Tachycardia (QRS width less than 120ms and Heart Rate more than 100bpm)
Three examples of Supraventricular Tachycardia include
- Atrial Fibrillation
- AV Re-entry Tachycardia
- AV Nodal Re-entry Tachycardia
What 4 Adverse Effects warrant DC Cardioversion in Supraventricular Tachycardia?
HISS
Heart Failure
Ischaemia
Shock
Syncope
How is Supraventricular Tachycardia managed in Stable Patients?
Regular (2)
Irregular
It depends on whether the arrhythmia is regular or irregular
Regular- Vagal Manoeuvres such as Carotid Sinus Massage or the Valsalva Manoeuvre should be attempted. If not, IV Adenosine 6mg should be administered.
Irregular- manage according to Atrial Fibrillation management
What should patients be warned of before IV Adenosine is administered (3)?
Difficulty Breathing
Chest Tightness
Flushing
How should IV Adenosine 6mg be administered in Supraventricular Tachycardia?
It should be given rapidly over 1-3 seconds, followed by 20ml IV Saline bolus
If this fails, a second dose of Adenosine 12 mg can be administered, followed by another dose of 12mg
What are the 4 cautions and contraindications to the use of Adenosine?
IV Adenosine 3mg should not be administered to Heart Transplant patients, patients with Central Line Access and patients on medications that can potentiate the effects of Adenosine, such as Dipyridamole or Carbamazepine.
Asthma is a contra-indication to the use of Adenosine so Verapamil should be used instead
What are the 7 complications of Supraventricular Tachycardia?
Syncope
Deep Vein Thrombosis
Embolism
Cardiac Tamponade
Congestive Cardiac Failures
Myocardial Infarction
Death
What are the 7 signs of a Tension Pneumothorax?
Haemodynamic Instability (4)- Tachypnoea, Tachycardia, Hypotension and Raised JVP
Tracheal Deviation away from the Affected Side
Decreased Chest Expansion
Increased Resonance on Percussion
Decreased Breath Sounds
Decreased Vocal Resonance
Surgical Emphysema
What is the 5 step management of an Upper GI Bleed?
A to E assessment to start with, focussing on IV Resuscitation and Blood Transfusion (if Hb<7) with or without Platelets and Frozen Fresh Plasma (every 4th unit of blood)
- Over transfusion Increases Mortality therefore patients should NOT be transfused to a normal Haemoglobin
The patient should be Nil By Mouth and given Supplemental Oxygen
IV PPI may also be initiated
In Variceal Bleeding, IV Terlipressin and Antibiotics are used
Once it is stable, Upper GI Endoscopy is carried out to locate the source of the bleeding through (2) Adrenaline Injection and Ulcer Clipping
What are the causes of a Long QT Interval?
TIMMES
Toxins (4)- Clarithromycin, Anti-arrhythmics, Anti-psychotics and Tricyclic Antidepressants
Inherited- Congenital Long QT Syndromes such as Romano-Ward and Jervell and Lange-Nielson Syndromes
Ischaemia
Myocarditis
Mitral Valve Prolapse
Electrolyte Abnormalities such as Hypokalaemia and Hypocalcaemia
Subarachnoid Haemorrhage
What is the management of Torsades de Pointes in Stable and Unstable Patients?
Unstable (Haemodynamic Compromise)- DC Cardioversion
Stable- IV Magnesium Sulphate 2g over 1-2 minutes
What does Resting Tachycardia, Orthostatic Hypertension and Supine Hypertension suggest in an Upper GI Bleed?
Resting Tachycardia suggests a mild to moderate hypovolaemia (less than 15% of blood loss)
Orthostatic Hypertension suggests at least 15% blood volume loss
Supine Hypotension suggests over 40% blood volume loss
What are the 6 causes of an Upper GI Bleed?
Oesophageal/ Gastric Varices
Peptic Ulcer Disease (H. pylori, NSAID use, Smoking)
Malignancy
Aorto-enteric Fistula (previous Abdominal Aortic Aneurysm or an Aortic Graft)
Angiodysplasia
Mallory Weiss Tear
What is the management of stable Ventricular Tachycardia?
IV Amiodarone
If the HISS Features (Heart Failure, Ischaemia, Shock, Syncope) are present, patients should be offered DC Cardioversion
What is the 5 step management of an Upper GI Bleed?
A to E assessment to start with, focussing on IV Resuscitation and Blood Transfusion (if Hb<7) with or without Platelets and Frozen Fresh Plasma (every 4th unit of blood)
- Over transfusion Increases Mortality therefore patients should NOT be transfused to a normal Haemoglobin
The patient should be Nil By Mouth and given Supplemental Oxygen
IV PPI may also be initiated
In Variceal Bleeding, IV Terlipressin and Antibiotics are used
Once it is stable, Upper GI Endoscopy is carried out to locate the source of the bleeding through (2) Adrenaline Injection and Ulcer Clipping
According to the Rockall Score, what 7 features warrant a Oesophago-Gastro-Duodenoscopy in an Upper GI Bleed?
Age higher than or equal to 60
Systolic Blood Pressure> 100
Heart Rate> 100
Cardiac Failure
Liver Failure
Renal Failure
Blood in Upper GI (seen in Endoscopy) or Upper GI Malignancy
What are the two scoring systems used to decide whether a patient needs Oesophago-Gastro-Duodenoscopy in an Upper GI Bleed?
Glasgow Blatchford Score
Rockall Score
What is Ventricular Tachycardia?
It is a Broad Complex Tachycardia (QRS Width>120ms) and HR>100
2 Other Types of Broad Complex Tachycardias include Torsades de Pointes and Supraventricular Tachycardia with Aberrant Conduction
What are the 4 causes of Ventricular Tachycardia?
Electrolyte Abnormalities (Hypokalaemia and Hypomagnesaemia)
Structural Heart Disease (Myocardial Infarction or Hypertrophic Obstructive Cardiomyopathy)
Drugs that cause QT Prolongation (Clarithromycin and Erythromycin)
Inherited Channelopathies (Romano-Ward Syndrome and Brugada Syndrome)
What is the management of stable Ventricular Tachycardia?
IV Amiodarone
If the HISS Features (Heart Failure, Ischaemia, Shock, Syncope) are present, patients should be offered DC Cardioversion
What are the 5 complications of Acute Kidney Injury?
Hyperkalaemia
Pulmonary Oedema
Metabolic Acidosis leading to Nausea, Vomiting and Drowsiness
Chronic Kidney Disease
Death
What are the 3 signs of an Acute Kidney Injury?
Increase in Serum Creatinine of 26micromol/L within 48 hours
Or an increase in Serum Creatinine at least 1.5 times above the baseline value within 1 week
Or urine output less than 0.5ml/kg/hour for more than 6 consecutive hours
What are the 3 Different approaches to treating Acute Kidney Injury?
Either Find and Treat the Causes (Sepsis, Drugs, Obstruction)
Or Stop the Renotoxic Drugs
Or Give IV Fluids, Treat the Complications and Dialyse
What are the 6 complications of an Addisonian Crisis?
Low Blood Pressure
Vomiting and Diarrhoea
Dehydration
Shock
Coma
Death
What are 5 Renotoxic Drugs?
ACE Inhibitors/ ARBs
Spironolactone
Diuretics
Gentamicin
NSAIDs
What are the 5 indications for Dialysis in Acute Kidney Injury?
Persistently high Potassium that is refractory to medical treatment
Severe Acidosis (pH<7.2)
Refractory Pulmonary Oedema
Symptomatic Uraemia (Pericarditis, Encephalopathy)
Drug Overdose (Aspirin)
What are the 5 complications of Acute Kidney Injury?
Hyperkalaemia
Pulmonary Oedema
Metabolic Acidosis leading to Nausea, Vomiting and Drowsiness
Chronic Kidney Disease
Death
What is an Addisonian Crisis?
It is the body’s inability to produce a sufficient amount of Cortisol
What is the 5 step management of an Addisonian Crisis?
Fluid Resuscitation if Hypotensive
IV Hydrocortisone 100mg (stat and then regularly)
IV Glucose if they are Hypoglycaemic
Swap back to their Prescribed Oral Steroids after 3 days
Consider Fludrocortisone if there is an Adrenal Disease
What are the 6 complications of an Addisonian Crisis?
Low Blood Pressure
Vomiting and Diarrhoea
Dehydration
Shock
Coma
Death
What are the 7 causes of Encephalitis?
Herpes Simplex Virus (most common cause)
Cytomegalovirus
Adenovirus, influenza virus
Tuberculosis
Listeria
Fungal (Cryptococcosis, Coccidiomycosis, Histoplasmosis)
Tick-borne Encephalitis
What are the 7 features of Encephalitis?
Fever
Headache
Altered Mental State
Personality Change
Focal Neurological Deficits
Convulsions
HSV1 Encephalitis is associated with Temporal Lobe Involvement so patient may experience Olfactory Symptoms (smell of Rotten Eggs)
What 3 investigations should be ordered if Encephalitis is suspected? What would they show?
CT Imaging (Medial Temporal and Inferior Frontal Lobe involvement with Petechial Haemorrhages seen in HSV Encephalitis)
MRI should also be performed after CT
Lumbar Puncture with CSF Analysis- Microscopy and Serology cultures needed to diagnose Encephalitis
What is the management of Encephalitis?
IV Aciclovir and IV Ceftriaxone to cover for bacterial infections
What are the 7 causes of Encephalitis and the most common cause of Encephalitis?
Herpes Simplex Virus (Most common cause)
Cytomegalovirus
Adenovirus/ Influenza Virus
Tuberculosis
Listeria
Fungal Causes (3)- Cryptococcosis, Coccidiomycosis, Histoplasmosis
Tick-borne Encephalitis
What are the 7 signs of Encephalitis?
Fever
Headache
Altered Mental State
Personality Change
Focal Neurological Deficits
Convulsions
HSV1 is associated with Temporal Lobe Involvement. So the patient may experience Olfactory Seizures such as the Foul Smell of Rotten Eggs
What 3 investigations should be ordered if Encephalitis is suspected? What would they show?
CT Scan- Medial Temporal and Inferior Frontal Lobe Involvement with the presence of Petechial Haemorrhages in HSV Encephalitis
MRI should be performed after
Lumbar Puncture with CSF Analysis- Microscopy, Serology and Cultures is needed to diagnose Encephalitis
What is the management of Encephalitis?
IV Aciclovir and IV Ceftriaxone
What are the 4 most common symptoms of an Acute Pulmonary Oedema? What are the 5 signs of Fluid Overload seen in Acute Pulmonary Oedema?
Extreme Dyspnoea
Restlessness
Anxiety
Bilateral Reduced Air Entry
Inspiratory Crepitations
Raised JVP
S3 Gallop
Peripheral Oedema
What are the 7 signs of Aspirin Overdose?
Nausea and Vomiting
Tinnitus
Fever
Confusion
Tachycardia
Initial Respiratory Alkalosis (caused by activation of respiratory centres in the brain)
Later Metabolic Acidosis (caused by wasting of bicarbonate ions due to the ingested acid load)- this is often mixed with the respiratory alkalosis
Which 2 investigations should be ordered for the diagnosis of Aspiring Overdose?
Venous Blood Gases- look for acid-base imbalances
Salicylate levels
What is the 4 step management of Aspirin Overdose?
Activated Charcoal if Ingestion< 1 hour ago
IV Fluid, Sodium Bicarbonate and Potassium Chloride
- (The aim is to maintain good kidney function and to alkalise the urine in order to increase Salicylate Excretion)
- Monitor with Serial Venous Blood Gases
Dialysis- may be necessary if blood levels are high
Monitor them for complications (3)
- Renal Functions
- Chest X-ray: Pulmonary Oedema
- CT Head: if Signs of Cerebral Oedema
What are the 3 main precipitants for Acute Pulmonary Oedema?
Cardiac Ischaemia
Arrhythmias
Non-compliance with Heart Failure Medication
What 6 investigations should be ordered if Acute Pulmonary Oedema is suspected?
Bedside Investigations
Arterial Blood Gases
ECG
Troponin- if there is concern for a new cardiac event
Serum BNP
Chest Xray
What is the 7 step management of an Acute Pulmonary Oedema?
Take an ABCDE Approach
Sit the patient up
Administer Oxygen
Ensure IV Access
IV Furosemide
Consider Non-Invasive Ventilation such as CPAP if failed medical therapy
Consider further therapies in the intensive care setting such as invasive ventilation and inotropic support if the above fails
How are patients with both Heart Failure and Renal Impairment managed? (4)
Acute Kidney Injury is largely Pre-renal due to Under-perfusion, which can be managed by Replacing Fluids as most patients are Hypovolaemic
But if patients have Heart Failure as well as Acute Kidney Injury, the Under-perfusion is because of a poor output from the heart
According to the Starling Curve, when the Left Ventricle End-diastolic Volume is too high, the Stroke Volume falls. This is what happens in Heart Failure patients with Fluid Overload
So by Off-loading fluid with Diuresis, the Stroke Volume improves, there is a greater output from the heart, so perfusion to the kidneys improve. Overall, when there is Elevated Central Venous Pressure, the Renal Function may recover with the aid of Diuresis
How are patients with both Heart Failure and Hypotension managed? (4)
The use of Diuretics to treat Heart Failure would be detrimental to the patient’s Hypotension- this can severely impact the perfusion of vital organs
In patients with Heart Failure and a Low Left Ventricular Ejection Fraction, if the Systolic Blood Pressure is low (<85mmHg) or the patient is in Shock (Confusion/ Cold Extremities), then add an Inotrope after discussing with a senior colleague.
- Small Fluid challenges of 250ml boluses over 15-20 minutes can be given to keep the blood pressure above 90mmHg and this needs to be carefully titrated
Vasopressors (Noradrenaline) may play a role in patients with Heart Failure with Persistent Hypotension, alongside evidence of End-organ Hypoperfusion. But only give Vasopressors if the response to Inotropes is insufficient
These measures are only temporary and aim to maintain perfusion to the End-organs until the Acute Trigger for the deterioration (the original cause of it) has been reversed, or a Definitive Treatment (Coronary Revascularisation, Mechanical Circulatory Support or Heart Transplantation) has been employed.
What is the definition of Syncope and Seizure?
Syncope is an acute transient loss of consciousness with a lot of Postural Tone
Seizures arise from a Sudden Synchronous discharge of Electrical Activity from neurons in the brain
What 5 factors are different in Syncope and Seizure?
Risk Factors-
- Syncope (3)- Heart disease (Arrhythmias), Peripheral Neuropathy, Drugs that cause Postural Hypotension (Diuretics, Antipsychotics, Antidepressants, Antihypertensives)
- Seizures (3)- Family or previous history of Epilepsy, Head Injuries, CNS Infections
Triggers-
- Syncope (5)- Pain, Heat, Exertion, Prolonged Standing, Emotion
- Seizures (4)- Alcohol, Sleep Deprivation, Bright Lights, Infections
Before the Episode-
- Syncope (4)- Dizziness, Light-headedness, Nausea, Tunnel-vision
- Seizures (4)- Aura: Strange Feelings like Epigastric Rising, Deja Vu, Visual or Smell Disturbances
During the Episode-
- Syncope (4)- Sudden loss of tone, May have tongue biting, May have incontinence, Brief Duration
- Seizures (4)- Tonic-clonic Jerking, May have tongue biting, May have incontinence, Brief or Prolonged Duration
After the Episode-
- Syncope- Complete and Rapid Recovery
- Seizures (2)- Post-ictal Confusion and Drowsiness, May have Todd’s Palsy- Focal Weakness after Seizure
What are the 3 main causes of Syncope?
Cardiac Pathology (3) (Arrhythmias, Valvular Disease, Cardiomyopathies)
Postural Hypotension (3) (Drugs, Volume Depletion, Autonomic Dysfunction)
Neurogenic Causes (Vasovagal Syncope)
What are the 5 main causes of Seizures?
Infections (2)- Meningitis, Encephalitis
Electrolyte Disturbances (6)- Hyponatraemia, Hypernatraemia, Hypoglycaemia, Hypocalcaemia, Hypokalaemia, Ammonia (Hepatic Encephalopathy)
Drugs (3)- Tricyclic Overdose, Alcohol and Benzodiazepine Withdrawal
Neurological Causes (4)- Stroke, Mass Lesions, Degenerative Conditions, Epilepsy
Obstetrics (Eclampsia)
What are Breakthrough Seizures?
Seizures which occur in known Epileptics
Can be caused by (4)- Poor medication compliance, Sleep deprivation, Alcohol, Stress
What 4 investigations should be ordered if an Acute Seizure?
Arterial Blood Gases (Hypoxia and Hypercapnia- look for these in Acute Prolonged Seizures)
Blood Tests (4) (FBC, U&Es (Serum Calcium, Magnesium, Phosphate), LFTs, Glucose)
Urine Test- Urine Toxicology Screen
Imaging- CT Head
What are the 8 signs of Digoxin Poisoning?
Dizziness
Nausea and Vomiting
Palpitations (due to Arrhythmias)
Bradycardia (usually Without Hypotension)
Yellow-Green Colour Disturbance
Visual Haloes
Confusion
Hyperkalaemia (but HypOkalaemia is a Risk Factor for Digoxin Poisoning)
What is the 5 step management for Digoxin Poisoning?
Measure the Immediate Digoxin Level
IV Fluids
Correct Electrolyte Abnormalities
Continuous Cardiac Monitoring
Give Digibind if (3)
- Digoxin Level >15ng/ml after 6 hours of last dose
- Digoxin Level >10ng/ml within 6 hours of last dose
- Symptomatic
What are the 9 signs of Hypoglycaemia?
Shaking/ Trembling
Sweating
Palpitations
Hunger
Headache
Double Vision and Difficulty Concentrating
Slurred Speech
Confusion
Coma
What are the Drug (6) and 5 other causes of Hypoglycaemia?
Drugs-
- Insulin
- Sulphonylureas
- GLP-1 analogues
- DPP-4 inhibitors
- Beta blockers
- Alcohol
Acute Liver Failure
Sepsis
Adrenal Insufficiency
Insulinoma
Glycogen Storage Disease
What 5 investigations may be ordered in Hypoglycaemia?
Check the Medication History for Drug Causes
Serum Insulin, C-peptide and Proinsulin- to Distinguish the Presence of Exogenous and Endogenous Insulin
(High Insulin and High C-peptide and Proinsulin= Endogenous Production/ High Insulin and Low C-peptide and Proinsulin= Exogenous Administration)
72 hour Fast Test- to demonstrate Episodic Hypoglycaemia
8am Cortisol and/ or synACTHen testing- for Adrenal Insufficiency
Abdominal CT/MRI/ PET- to look for an Insulinoma
How is Mild (still conscious) and Severe (seizures, unconscious) Hypoglycaemia managed? (4,4)
Mild Hypoglycaemia
- ABCDE
- Eat/drink 15-20g Fast-acting Carbohydrate such as Glucose Tablets, a small can of Coca Cola, Sweets or Fruit Juice
- AVOID Chocolate
- Eat some Slow-acting Carbohydrate afterwards (toast)
Severe Hypoglycaemia
- ABCDE
- 200ml 10% Dextrose IV
- 1mg/kg Glucagon IM- if there is no IV access (this will NOT work if the Hypoglycaemia is caused by Acute Alcohol as it blocks Gluconeogenesis)
- Treat Seizure if Prolonged or Repeated
After Care- (2)
- Consider Medication Changes
- Investigate non-drug causes if necessary
What is Pheochromocytoma?
It is a Tumour in the Adrenal Medulla that secretes Catecholamines (Hormones produced by Adrenal Glands such as Noradrenaline)
If it arises in Sympathetic Nerve Tissue, it is called a Paraganglioma
What are the 14 symptoms of Pheochromocytoma?
Pyrexia
Dyspnoea
Hypertension
Postural Hypotension
Tremor
Hypertensive Retinopathy
Abdominal pain
Anxiety
Weight loss
Fatigue
Palpitations
Sweating
Headaches
Flushing
What 5 things Precipitate the Symptoms of Pheochromocytoma?
Stress
Exercise
Surgery
Straining and Various Drugs such as Beta Blockers
Anaesthetic Agents and Opiates
What investigations should be ordered if Pheochromocytoma is suspected? (6)
Plasma Metanephrines and then Urinary Metanephrines have the best Diagnostic Accuracy to Establish a Catecholamine Excess
24 Hour Urinary Catecholamines can be measured as well however they are of less value
Adrenal Imaging should not take place until the Biochemical Diagnosis has been confirmed
CT Chest Abdominal and Pelvis imaging is the imaging method of choice and should be followed with an MRI Scan (as an Extra-adrenal Pheochromocytoma can occur anywhere from the Base of the Brain to the Bladder as it develops in the Chromaffin Tissue of the Sympathetic Nervous System)
PET Scans can also help
Other tests include Metaiodobenzylguanide (MIBG) labelled with Iodine (which has a similar composition to Noradrenaline)
What is the 3 step management of Pheochromocytoma?
The definitive treatment is to Surgically Resect the Tumour
Pre-operatively, Alpha Blockade with Phenoxybenzamine is started First
This is followed by Beta Blockade to Expand the Blood Volume. This is to Expand the Blood Volume and Prevent a Hypertensive Crisis
What are the signs of Acute Spinal Cord Compression? (5)
Upper Motor Neuron Signs
Sensory Disturbance below the level of the lesion
Deep localised Back Pain may also be present
Also a Stabbing Radicular Sensory Disturbance at the Level of the Lesion
Bladder and Bowel Involvement may also be seen
What are the 5 causes of Acute Spinal Cord Compression?
Trauma
Neoplasia (Spinal Cord Compression is seen in 5-10% of Cancer patients, and is the presenting complaint in 20% of them)
Infection (especially Tuberculosis in at-risk patient)
Disc Prolapse
Epidural Haematoma
What is the management of Acute Spinal Cord Compression? (2)
They should have a URGENT Whole Spine MRI with an aim to Surgically Decompress within 48 hours
If there is a Malignancy seen on MRI, or if the Clinical Suspicion of a Malignancy is high, Dexamethasone 16mg daily should be Administered- with PPI Cover
What is a Thyrotoxic Storm?
It is a life-threatening, hypermetabolic state caused by an excessive release of Thyroid Hormones
What are the 3 symptoms of a Thyrotoxic Storm?
High Blood Pressure
High Temperature
Tachycardia
What is the 3 step management of a Thyrotoxic Storm?
Symptom Control (2)
- IV Propanolol
- IV Digoxin if Propanolol fails or is Contraindicated (Asthma, low BP)
Reduce Thyroid Activity (4)
- Propylthiouracil through an NG tube- (preferred as it inhibits peripheral thyroxine conversion)
- Lugol’s iodine 4 hours later
- Methimazole/ Carbimazole is considered second line
- IV Hydrocortisone/ Prednisolone to reduce Thyroid Inflammation
Treat Complications (Heart Failure, Hyperthermia)
What are the 9 causes of Secondary Epistaxis?
Alcohol
Antiplatelet Agents (Clopidogrel)
Aspirin and NSAIDs
Anticoagulants (Warfarin)
Coagulopathy (2)- Haemophilia, von Willebrand’s Disease
Trauma (Nasal Fracture)
Tumours
Surgery
Septal Perforation
What is the general approach to treating Epistaxis?
DRABCDE
Brief history- which side? trauma? anticoagulants/ antiplatelets? relevant past medical history?
What are the 4 specific management approaches to Epistaxis? (2,4,2,1)
Direct Compression
- Direct Compression of the Nasal Alae (Cartilage part) is the First Line Management as most Anterior Nose bleeds resolve after 10-15 minutes of compression. Patient should be Sitting up and Leaning Forward. Compression of the Nasal Bones isn’t what controls the bleeding
- If this does not resolve the bleed, the next step is Cautery, especially if there is a Visible Bleeding sight and the patient suffers from Recurrent Nose Bleeds
Cautery-
- Before Cautery, a Topical Anaesthetic Spray and Vasoconstrictor (Lidocaine with Phenylephrine) is applied to Reduce the Pain and Help Control the Bleeding respectively
- Cautery can be Chemical or Electrical (Thermal)
- Chemical Cautery involves applying 75% Silver Nitrate sticks to the identified bleed for 3-10 seconds
- Afterwards, the cauterised area is dabbed with a clean cotton bud to remove excess Chemical and Blood. A Topical Antiseptic preparation such as Naseptin (Chlorhexidine and Neomycin) is applied to the nostrils 4 times a day for 10 days to reduce Crusting and Vestibulitis
Nasal Packing-
- If Nasal Cautery fails or if there isn’t a Bleeding Point or if there is Severe Bleeding, Nasal Packing should be attempted
- Nasal Tampons, Inflatable Packs and Ribbon Gauze Impregnated with Vaseline can be used in Nasal Packing
Aggressive Therapies-
- Nasal Balloon Catheter and Transnasal Endoscopy with Direct Cautery/ Arterial Ligation are reserved for patients with Posterior Bleeds and Uncontrollable Severe Bleeding unamenable to Nasal Packing
What is Glandular Fever?
Also known as Infectious Mononucleosis- it is caused by the Epstein-Barr Virus. It is transmitted by saliva which is why it is known as the Kissing Disease
What are the 4 main symptoms of Glandular Fever?
Fever
Sore throat
Fatigue
Hepatomegaly and/or splenomegaly may be found on palpation
What is the diagnosis and management of Glandular Fever?
The diagnosis is usually made clinically although the heterophile antibody “Paul Bunnell” test will be positive
Management is supportive and patients are advised against contact sports and heavy lifting for 1 month to minimise the risk of Splenic Rupture
What are the 11 risk factors for a Haemorrhagic Stroke?
Age
Male Sex
Family History of a Haemorrhagic Stroke
Haemophilia
Cerebral Amyloid Angiopathy/Hypertension
Anticoagulation Therapy
Illicit Sympathomimetic Drugs (Cocaine and Amphetamines)
Vascular Malformations (particularly in younger patients)
Non-steroidal Anti-inflammatory Drugs
Heavy Alcohol Use
Thrombocytopaenia
What is the 3 step management of a Haemorrhagic Stroke?
Neurosurgical and Neurocritical Care Evaluation due to the potential for surgical intervention (Decompressive Hemicraniectomy)
Admission to the Neuro ICU or Stroke Unit (patient may require Intubation and Ventilation or Invasive monitoring of ICPs)
Aim to keep Blood Pressure <140/80 as poor blood pressure control in the acute stage is associated with poorer outcomes later on
What are the 3 causes of Horner’s Syndrome?
Pancoast Tumour (Affecting Sympathetic Nerve Supply)
Stroke
Carotid Artery Dissection (Red flag: Neck Pain)
What are the 3 symptoms of Horner’s Syndrome and what is the pathophysiology?
Ptosis
Meiosis
With or Without Anhidrosis
It occurs due to the interruption of the Sympathetic Nerve Supply to the eye and can be classified into Pre-ganglionic, Central and Post-ganglionic causes
What are the 4 Peripheral Features, 2 Head and Neck Features, 5 Eye Features, 2 Cardiac Features, 1 Gastrointestinal Feature and 2 Neurological Features of Hyperthyroidism? (6 type of features altogether)
Peripheral Features-
- Fine Tremor
- Finger Clubbing
- Sweating
- Pretibial Myxoedema
Head and Neck Features-
- Goitre (depending on the cause)
- Thyroid Bruit
Eye Features-
- Lid Retraction
- Lid Lag
- Exophthalmos (Graves’ Disease)
- Periorbital Oedema (Graves’ Disease)
- Ophthalmoplegia (Graves’ Disease)
Cardiac Features-
- Atrial Fibrillation
- High output Heart Failure (if severe and prolonged)
Gastrointestinal Features-
- Diarrhoea
Neurological Features-
- Muscle Wasting
- Proximal Weakness
What are the 6 primary causes and 7 secondary causes of Hyperthyroidism?
Primary Causes-
- Graves Disease
- Toxic Thyroid Adenoma
- Multinodular Goitre
- Silent Thyroiditis
- De Quervain’s Thyroiditis (Painful Goitre)
- Radiation
Secondary Causes-
- Amiodarone
- Lithium
- TSH-producing Pituitary Adenoma
- Choriocarcinoma (Beta HCG can activate TSH Receptors)
- Gestational Hyperthyroidism
- Pituitary Resistance to Thyroxine (the failure of the Negative Feedback Mechanism)
- Struma Ovarii (ectopic thyroid tissue in Ovarian Tumours)
What is prescribed for Symptom Relief in Hyperthyroidism, and what is prescribed as Medical Management in Hyperthyroidism (2)- which one is given in Pregnancy?
Propranolol is given for Symptom Relief
Carbimazole and Propylthiouracil are given for Medical Management of Hyperthyroidism
Carbimazole is contraindicated in Pregnancy, Propylthiouracil is given in the First Trimester in Pregnancy or in a Thyroid Storm
What is the indication and contraindication for Radioiodine in Hyperthyroidism?
Radioiodine is the definitive management for Multinodular Goitre and Adenomas
Radioiodine is Contraindicated in Graves Eye Disease as it may worsen the symptoms
What are the 3 indications and 4 complications for Thyroidectomy in Hyperthyroidism?
It is indicated for (3) Recurrence, Goitres that obstruct other structures and Potential Cancers
Complications- Hypoparathyroidism, Hypocalcaemia, Laryngeal Nerve Damage, Bleeding
What are the 7 complications of Hyperthyroidism?
Thyroid Storm (often precipitated by Trauma, Surgery or Infection)- this may present as (5)- High Fever, Tachycardia, Confusion, Nausea, Vomiting
Atrial Fibrillation
High output Heart Failure
Osteopenia/ Osteoporosis
Upper Airway Obstruction due to a Large Goitre
Corneal Ulcers/ Visual Loss in Graves’ Eye Disease
What are the 6 ECG Features of Hypothermia?
Bradyarrhythmias (4) (Sinus Bradycardia, Atrial Fibrillation with a Slow Ventricular Response, Slow Junctional Rhythms, Varying degrees of AV block)
Osborne Waves (J Waves)- a positive deflection at the J Point- between the end of the QRS and beginning of the ST Segment
Prolonged PR, QRS and QT Intervals
Shivering Artefact
Ventricular Ectopics
Cardiac Arrest (Ventricular Fibrillation, Ventricular Tachycardia or Asystole)- patients with hypothermia are at high risk of a Cardiac Arrest
How is Hypothermia Managed?
Cover Patients with a Warm Blanket and supply Warm Drinks
Passive Warming can be done through the Intravenous Admission of Warm Fluids and Application of Warm Air (like through a Bair-Hugger). Patients are at a high risk of Cardiac Arrest and CPR may be used
What is Idiopathic Intracranial Hypertension?
It results in an Intracranial Pressure (opening pressure> 25cmH2O)
It occurs commonly in Young and Obese Women
What are the Clinical Features of Idiopathic Intracranial Hypertension?
Headache and Visual Disturbance
The headache is Non-Pulsatile, Bilateral and Worse in the Morning and after Lying Down or Bending Forward
Visual Disturbances include Transient Visual Darkening or Loss- probably due to Optic Nerve Ischaemia. In Fundoscopy, Bilateral Papilloedema is seen. If left untreated, the visual loss may be permanent
Patients may even report Morning Vomiting. A Key Differential for Morning Headache in these Obese Patients is Sleep Apnoea
What 5 drugs are associated with Idiopathic Intracranial Hypertension?
Oral Contraceptive Pills
Steroids
Tetracyclines
Vitamin A
Lithium
What is the 4 step management of Idiopathic Intracranial Hypertension?
Weight Loss (First line and only intervention supported by good evidence)
Carbonic Anhydrase Inhibitors are given if this doesn’t work (Acetazolamide) but it has 3 side effects (Peripheral Paresthesia, Anorexia and Metallic Dysguesia). Topiramate and Furosemide can also be used
Invasive Strategies to lower CSF include Therapeutic Lumbar Punctures and Surgical CSF Shunting
In patients with prominent visual symptoms, Optic Nerve Fenestration may protect against visual loss
What are the 7 Criteria for performing a CT Head within 1 hour of a Head Injury?
GCS less than 13 on initial assessment in the emergency department
GCS less than 15 at 2 hours after the injury
Suspected Open or Depressed Skull Fracture
Any sign of Basal Skull Fracture (4) (Haemotympanum, Panda Eyes, Cerebrospinal Fluid Leak from the Ear or Nose, Battle’s Sign)
Post-traumatic Seizure
Focal Neurological Deficit
More than 1 episode of vomiting
What are the 4 Criteria for performing a CT Head within 8 hours of a Head Injury in patients who have experienced a Loss of Consciousness or Amnesia since the Injury?
Age 65 or older
Any history of Bleeding or Clotting Disorders
Dangerous Mechanism of Injury (struck by Motor Vehicle, Ejected from Motor Vehicle, fall from a height greater than 1 metre)
More than 30 minutes of Retrograde Amnesia of events immediately before the Injury
What are the 5 cardiac and 3 non-cardiac causes of Raised Troponin level
Cardiac Causes-
- Myocardial Infarction
- Arrhythmias
- Coronary Artery Spasms
- Aortic Dissections
- Severe Hypertension
Non Cardiac-
- Chronic Kidney Disease
- Pulmonary Embolism
- Sepsis
How are Head Trauma patients managed?
ABCDE Algorithm
Stabilising the C-Spine and Airway
Recognising Haemorrhage and Treating the Pain
What are the 8 signs of a Skull Fracture?
Subcutaneous Haematoma
CSF Rhinorrhoea (from the Anterior Nares (Nostrils))
CSF Otorrhoea (leakage of CSF from the External Auditory Meatus)
Subcutaneous Haematoma around the Orbits (Panda Eyes)
Haemotympanum
Subcutaneous Haematoma behind the Ear (Battle Sign)
Subcutaneous Emphysema
Cranial Nerve Palsies (arise 1-3 days after the Trauma)
What 2 interventions are contraindicated in Head Trauma?
Nasopharyngeal Airways are Contraindicated as they can cause further damage to the patients
Head tilt, Chin Lift is Contraindicated in Trauma patients at risk of a C-Spine Injury
What 4 investigations are ordered in Head Trauma?
First line is Plain CT Head
CT Cervical Spine to look for Spinal Fractures
CT Angiogram to look for Local Vascular Injuries
Plain Skull Xray to look for Orbital Fractures
How is Neisseria Meningitidis spread?
Respiratory Droplet Spread
The pathology is triggered when the bacteria enters the circulation, initiates the inflammatory process leading to capillary leakage and intravascular thrombosis
What is the presentation of a Meningococcal Infection? (5)
Meningococcaemia (Septicaemia)
Meningitis (non-specific signs such as (5) Lethargy, Headache, Fever, Rigors and Vomiting)
A mixture of both Meningitis and Meningococcaemia associated with a Rapidly Developing Purpuric Skin Rash
Hypovolaemic Shock may present with (4) Cold Peripheries, Poor Capillary Refill Time and Tachycardia, with Decreased Urine Output
When this is associated with Massive Adrenal Haemorrhage and Septic Shock, the presentation is known as Waterhouse-Friderischsen Syndrome. This is rare
How can the diagnosis of a Meningococcal Infection be confirmed? (2)
Blood or CSF Cultures
Polymerase Chain Reaction Testing for Neisseria Meningitidis is highly sensitive
What is the 3 step management of a Meningococcal Infection?
Early Antibiotic Treatment should be given. This will usually be Broad Spectrum IV Antibiotics until confirmation of the pathogen, after which antibiotics may be narrowed to Penicillin-based drug if Sensitivities permit
Patients are likely to need PICU admission is Septicaemia
Infections caused by Neisseria meningitidis are notifiable diseases
What 2 thing should be done to prevent Menignococcal Infections?
All household or close contacts should receive Ciprofloxacin or Rifampicin as Post-exposure Prophylaxis
Multiple strains of Neisseria Meningitidis covered as part of the Routine Immunisation Schedule
What is the 8 step management of a Myxoedema Coma?
ITU/ HDU care
IV T3/ T4
50-100mg IV Hydrocortisone
Mechanical Ventilation and Oxygen (if Hypoventilation)
IV Fluid- to correct Hypovolaemia
Correct Hypothermia
Correct Hypoglycaemia
Treat any Heart Failure
What is Necrotising Fasciitis?
It is a life-threatening infection of the subcutaneous soft tissue, which spreads along the fascial planes but not the underlying muscle
What is the presentation of Necrotising Fasciitis?
Rapidly spreading cellulitis and patients are systemically unwell. There is often a history of risk factors (cutaneous portal of entry for bacteria, like Trauma or Surgery)
On physical examination- the affected region will be Blistering and Erythematous. But a Mild Oedema may be the only sign. There will be severe pain or anaesthesia over the site of Cellulitis. In advanced stages, the skin may be grey with overlying Crepitus. The patient is typically (4) Pyrexial, Tachycardic, Tachypnoeic and Hypotensive
How is Necrotising Fasciitis managed (3, 1)?
Haemodynamic Support
Urgent Debridement Surgery
Broad Spectrum Antibiotics
Radiography or CT/MRI can confirm the diagnosis but should not delay the surgery
What are the 4 causes of Oesophagitis?
Reflux of Gastric Contents
Drugs
Infections
Allergens (Eosinophilic Oesophagitis)
What are the 3 symptoms of Oesophagitis?
Heartburn (retrosternal burning pain)
Nausea and Vomiting
Odynophagia (painful swallowing)
What 3 investigations can be conducted if Oesophagitis is suspected?
Endoscopy allows for a direct visualisation of the Oesophagus and can be used to Grade the degree of Oesophagitis (Savary-Miller Grading System, Los Angeles Grading System)
Biopsy can be taken with the Endoscopy
If reflux is suspected as the cause, Oesophageal pH monitoring can be used to identify whether the timing of the symptoms and the reflux correlates
What is the management of Oesophagitis?
As reflux is the most common cause,
- Lifestyle changes such as (3) Weight loss, Stopping smoking and Reducing Alcohol intake and…
- Pharmacological treatment such as Protein Pump Inhibitors can be administered
What two bones are most at risk for an Open Fracture?
the Tibia and the Phalanges
What is the 3 step management of an Open Fracture? (1, 2, 2)
The Prompt Administration of Antibiotics (open fractures are at risk of infection)
Debridement and Irrigation
Reduction and Fixation
What are the 8 signs of Paracetamol Overdose?
No symptoms may be present
Nausea and Vomiting
Loin Pain
Haematuria and Proteinuria
Jaundice
Abdominal Pain
Coma
Severe Metabolic Acidosis
What is the pathophysiology of Paracetamol Overdose?
When overdosed, the metabolism of Paracetamol results in a buildup of a toxic substance called NAPQI (N-acetyle-p-benzoquinone-imine)
NAPQI is inactivated by Glutathione usually, however in an overdose, the Glutathione stores are rapidly depleted and NAPQI damages the Kidneys and Livers
What is the management of Paracetamol Overdose (6)?
If the ingestion is less than 1 hour ago and the dose is greater than 150mg/kg- Administer Activated Charcoal
If they had a Staggered Overdose (duration of overdose>1 hour) or ingestion was more than 15 hours ago or there is any uncertainty about the timing- Start N-acetylcysteine immediately
If ingestion <4 hours ago, wait until 4 Hours to take a level (blood paracetamol level) and treat with N-acetylcysteine based on their level (refer to a Nomogram)
If ingestion is 4-15 hours ago, take an immediate level and treat based on their level
Obtain bloods for (4)- FBC, Urea and Electrolytes, INR and Venous Gases
Consider the need for transfer to Liver Unit if blood tests are Worsening
What is N-Acetylcysteine associated with?
Anaphylactoid Reactions. These are not true Anaphylactic Reactions and can be managed by stopping the Infusion Temporarily and restarting at a Lower Rate
What are 4 things that increase the risk of Paracetamol Toxicity in patients and means the patients should be immediately administered N-acetylcysteine?
Patients on long-term Enzyme Inducers
Regular Alcohol Excess
Pre-existing Liver Disease
Glutathione-deplete States- Eating Disorders, Malnutrition and HIV
What are 5 different signs of Type A Dissections (Ascending Aorta and Aortic Arch) and 3 signs of Type B Dissections (Descending Aorta)? Where is the dissection according to each sign? (in brackets)
Type A
- Central chest pain (Coronary Ostia- leads to Myocardial Infarction)
- Dyspnoea (Ascending Aorta- leads to Aortic Regurgitation and therefore Congestive Heart Failure)
- Neck/ Jaw Pain (Aortic Arch)
- Horner’s (Cervical Sympathetic Ganglia)
- Symptoms of Stroke (Carotid Arteries)
Type B
- Interscapular pain (Thoracic Descending Aorta)
- Abdominal pain (Abdominal Descending Aorta or Mesenteric Arteries)
- Flank pain (Renal Arteries)
What is the difference between the intensity of the pain in Aortic Dissection and Myocardial Infarction?
Aortic Dissection pain is worst at onset and gets better
Myocardial Ischaemia pain gets worse as the Ischaemia Worsens
What are the 2 differential diagnoses for Seizures in Adult Patients?
Syncopal Episodes and Pseudoseizures
What are the features of a Generalised Seizures?
Sudden Onset
Lateral tongue biting and Urinary Incontinence may occur. After the event, the patient is usually confused (but may recall the onset especially if secondary generalised seizure). They may be left with a residual focal neurological deficit (Todd’s Paresis)
There are two groups of Seizures- Provoked and Unprovoked Seizures, where there is an underlying tendency to spontaneous abnormal electrical brain activity (which manifests clinically as seizures), these may be Congenital or Acquired Tendencies
What are the features of Syncope?
The Absence of Postictal Confusion. With Vasovagal Syncope, patients report (3) Narrowing of Vision, Sweating and Lightheadedness and have time to safely lower themselves onto the floor.
Arrhythmogenic Syncope (Stokes-Adams attacks) are abrupt in onset without any warning and may result in significant injury. Myoclonic Jerks or Tonic Posturing may occur during these episodes which may confound diagnosis
What are the features of Pseudoseizures?
They are called Psychogenic NonEpileptic Attacks. They are often Prolonged Episodes (rarely< 1 minute, often> 30 minutes)
The patient often has Seizure-like Convulsions and Fluctuating Motor Activity.
Video EEG Recording helps to differentiate Pseudoseizures from True Seizures
Differential Diagnoses include Hemiplegic Migraine and Cerebrovascular Events, although Consciousness is typically preserved in Pseudoseizures
If patients have True Seizure Activity and Focal Weakness, differentiating Seizure plus Todd’s Paresis from Stroke plus Seizure Onset is difficult clinically and Requires Imaging
What are the 2 types of Seizures?
Focal (or Partial Seizures) may spread to involve the entire brain- these are called Secondary Generalised Seizures. Focal Seizures may be subclassified on the basis of Key Clinical Features, in particular the part of the brain that they involve (Temporal vs. Frontal lobe seizures) and whether consciousness is impaired (Simple vs. Complex)
The clinical manifestation of a Generalised Seizure may be described. These are either (4) Tonic, Tonic-Clonic, Myoclonic or Absence. Generalised Tonic-Clonic (or Grand Mal) seizures are the most typical- the patient falls to the ground (Tonic) and has rhythmic jerks (Clonic Absence)
What determines whether a patient has Systemic Inflammatory Response Syndrome (SIRS)?
2 or more of:
- > 38 degrees or <36 degrees temperature
- Heart Rate>90 (not 100 like Tachycardia)
- Respiratory Rate>20
- WBC> 12,000/mm cubed or <4,000/mm cubed
What determines whether a patient has Sepsis?
SIRS and a presumed Infection
What determines whether a patient has Severe Sepsis?
Sepsis and evidence of Organ Dysfunction (4)- Confusion, Hypoxia, Oliguria, Metabolic Acidosis
What determines whether a patient has Septic Shock?
Severe Sepsis with Hypotension despite (3) Adequate Fluid Resuscitation or Lactic Acidosis (Lactate>3mmol/L)
What are the 11 signs of Sepsis?
- Fever, Sweats or Chills
- Breathlessness
- Headache
- Nausea and Vomiting
- Diarrhoea
- Tachycardia
- Hypotension
- Pyrexia
- Peripherally Vasodilated
- Hypoxia
- Tachypnoea
What is the management approach to Sepsis? What 4 investigations should also be ordered and what 3 additional management steps should be carried out?
ABC (Airways, Breathing, Circulation) + Sepsis Six
- Take Bloods (FBC, U&Es, LFT, CRP, Lactate)
- Take Blood Cultures
- Administer Oxygen if required (Sats<94%)
- Administer IV Antibiotics
- Administer IV Fluid Resuscitation (Fluid Challenge- Crystalloid if (2) Systolic BP<90mmHg or Lactate>4mmol/L and high risk of Sepsis)
- Catheterisation and monitor urine output
4 Investigations-
- Imaging (CXR, Echocardiogram, Abdominal Ultrasound)
- Viral PCR for any viruses like Influenza for example
- Urinalysis, with or without Culture
- Lumbar Puncture
Ongoing Management (depends on the Source and the Severity)
- IV Antibiotic Therapy
- Surgical Removal of Source of Infection
- Critical Care Involvement
What is the Triad of Serotonin Syndrome and what causes it?
Mental State Changes
Autonomic Hyperactivity (arousal of the sympathetic nervous system typically- results in signs of Anxiety (5)- Sweating, Lightheadedness, Dry Mouth, Palpitations, Upset Stomach
Neuromuscular Abnormalities (muscle weakness, paresthesia)
It usually presents within the first couple months of starting an SSRI or because of drug interactions like Tramodalol and Sertraline
What are the 6 types of Shock and their causes?
Hypovolaemic Shock (Blood Loss)
Septic Shock (Severe Systemic Infections)
Anaphylactic Shock (Allergy)
Cardiogenic Shock (Poor Cardiac Output)
Neurogenic Shock
Obstructive Shock (A Physical Obstruction of the Vessels or the Heart)
What is the management of Hypovolaemic Shock in Trauma? (5)
1.5-2L Warmed IV Crystalloid
Assess for response
If the response to the fluid is inadequate, arrange O Negative Blood
Give fully cross-matched blood as soon as possible
If the patient is Severely Shocked, initiate the Massive Haemorrhage Protocol
What are the features of Space Occupying Lesions (5)?
A Prominent Headache worse when (4) Waking up, Lying down, Coughing/ Straining and associated with Vomiting
Early symptoms of a Raised ICP are Non-specific and include a Headache associated with morning Nausea and Vomiting
Patients may have Cranial Nerve Palsies- especially within the Abducens Nerve
In Advanced Cases, Drowsiness and Seizure Activity may occur with Pupillary Abnormalities and Papilloedema
The Cushing’s Reflex may also be demonstrated where a patient has Raised Blood Pressure, Bradycardia and Abnormal Breathing (including Cheyne-Stokes Respiration)
What are the Differential Diagnoses of a Space Occupying Lesion? (4)
There are 4 types of Space Occupying Lesions (Tumours, Vascular Lesions, Infective Processes, Granulomata)
Space Occupying Neoplasia can occur secondary to Metastatic Disease (from Breasts, Lungs or Melanoma) or as a Primary CNS Tumour
Infective Processes include Cerebral Abscesses and rarer diseases such as Tuberculosis
Patients who are immunosuppressed are more prone to Intra-cerebral Infections so look for risk factors such as HIV
How are Space Occupying Lesions diagnosed?
Cranial MRI is more useful that Cranial CT
What 4 questions should you ask yourself if a patient presents with Sudden Painless Visual Loss?
What is the Time Course?
What are the associated symptoms?
What is the Medical History?
What does the Retina look like?
What are the 7 causes of Sudden Painless Visual Loss?
Central Retinal Vein Occlusion (More common than CRAO)
Central Retinal Artery Occlusion
Ischaemic Optic Neuropathy
Giant Cell Arteritis
Retinal Detachment
Vitreous Haemorrhage
Optic Neuritis
What are the Fundoscopy Findings and Risk Factors of Central Retinal Vein Occlusion (5) and Central Retinal Artery Occlusion (6)
Central Retinal Vein Occlusion (More common that CRAO)-
- Stormy Sunset Appearance on Fundoscopy
- Old Age
- Hypertension
- Diabetes
- Polycythaemia
- Arteriosclerosis
Central Retinal Artery Occlusion-
- Pale Retina with Cherry Red Spot at the Macula
- Carotid Bruit
- Hypertension
- Atrial Fibrillation
- Diabetes Mellitus
- Smoking
- Hyperlipidaemia
What are 3 facts each about Ischaemic Optic Neuropathy, Giant Cell Arteritis, Retinal Detachment, Vitreous Haemorrhage and Optic Neuritis?
Ischaemic Optic Neuropathy
- Optic Nerve Damage due to a lack of blood supply
- Different causes and so patients present differently, but generally have Sudden Onset Monocular Vision Loss and Colour Blindness
- Relative Afferent Pupillary Defect is seen on examination. On Fundoscopy, Optic Disc Swelling if it is acute and a Pale Optic Disc if it is chronic suggests Optic Atrophy
Giant Cell Arteritis
- Commonest form of Arteritic Anterior Ischaemic Optic Neuropathy
- Typically Elderly Female presenting with Sudden Onset Painless loss of vision with (3) Headache, Jaw Claudication and Scalp Tenderness
- There is a strong association between this condition and Polymyalgia Rheumatica
Retinal Detachment
- Patients present with Floaters and Flashers followed by a Curtain Falling over their Vision
- Don’t confuse this with Amaurosis Fugax which is the same as this but is Transient
- Fundoscopy shows a Pale-grey area of Retina Ballooning forward
Vitreous Haemorrhage
- If it is minor, patients complain of Floaters, if it is severe then patients complain of a Painless Loss of Vision
- When the bleed is large enough to cause visual loss, the retina is Difficult to View on Fundoscopy
- Suspect this is in patients with Neovascularisation in Diabetes Mellitus or Central Retinal Vein Occlusion
Optic Neuritis
- This is not a Sudden loss of vision as it progresses over Hours to Days- it is also Painful
- Suspect this if Ocular Movement causes pain or if there is a Red Desaturation
- Optic Neuritis is the most common initial feature of Multiple Sclerosis
What are the 2 main Surgical Complications? What 2 investigations should be ordered in Post-Surgery Patients with Symptoms? How should a Small (3) and Large Leak be managed?
An Anastomotic Leak- the Contents of a Hollow Organ which was joined Surgically leaks through a fault in the join
The bowel contents can leak and contaminate the Peritoneal Content and this can lead to (3) Peritonitis, Abscess Formation and Abdominal Sepsis
Suspect this in patients who have had an Intestinal Surgery and have (3) Failure to Thrive, a Persistent Low Grade Fever or Prolonged Ileus (lack of normal muscle contractions of the Intestine)
Radiological Investigations can be used to identify any Inappropriate Presence of IV Contrast in the Abdominal Cavity
Lactate Levels from a VBG can be used to assess Tissue Ischaemia. Patients require Investigations for Sepsis which is another Complication
A small leak can be managed conservatively with (3) Bowel Rest, IV Fluids and Antibiotics. They require repeated Abdominal Monitoring
Larger Leaks may require Emergency Laparoscopic Exploration with potential further Surgery
What are the parameters for the Glasgow Coma Scale?
Motor Score
6- Obeys Command
5- Localises to Pain
4- Withdraws to Pain
3- Flexor Response to Pain
2- Extensor Response to Pain
1- No Response to Pain
Verbal Score
5- Oriented
4- Confused Conversation
3- Inappropriate Speech
2- Incomprehensible
1- None
Eye Score
4- Spontaneous
3- Open in Response to Speech
2- Opens to Pain
1- No Eye Opening
GCS of 8 or Lower suggests the patient is unable to Maintain their own Airway and warrants urgent assessment by the Anaesthetic Team
What constitutes whether Bradycardia is a Medical Emergency? (4)
Systemic Hypotension
Signs of Cerebral Hypoperfusion
Progressive Heart Failure
Angina
What are the 8 causes of Bradycardia?
Normal in Athletic Individuals
Electrolyte Disturbances
Hypothyroidism
Myocardial Infarction
Sepsis
Drugs (Beta Blockers)
Increased Intracranial Pressure
Heart Block
How is Bradycardia managed? (3)
If there is evidence of Haemodynamic Compromise- Medical Therapy should be started immediately regardless of the cause
3 Medications used to increase Ventricular Rate are Intravenous Atropine, Epinephrine (Adrenaline) and Dopamine
Patients who do not respond to Medical Therapy require Temporary Pacing (2)- Transcutaneous and Transvenous Pacing are the most common types
What are the 8 signs of Tricyclic Antidepressant overdose?
Drowsiness
Confusion
Arrhythmias
Seizures
Vomiting
Headache
Flushing
Dilated Pupils
What 6 investigations should be ordered in Tricyclic Antidepressant overdose?
FBC
U&Es
CRP
LFTs
Venous Blood Gas (look for Evidence of Acidosis)
QT interval prolongation- which precipitates Cardiac Arrhythmias
How is Tricyclic Antidepressant Overdose managed?
Overall management is based on the patient’s symptoms
Patients should be reviewed by Intensive Care if (2) there is any concern about their Airway (especially if they are drowsy) or if there is Severe Metabolic Acidosis which may require Renal Replacement Therapy
Activated Charcoal can be considered 2-4 hours After the Overdose
What causes Wolff-Parkinson-White Syndrome?
It is due to a Congenital Accessory Electrical Pathway which connects the Atria to the Ventricles, bypassing the AV Node
This Accessory Pathway leads to the likelihood for Re-entrant Circuits to form leading to Supraventricular Tachycardia
What are the Symptoms of Wolff-Parkinson-White Syndrome?
No Symptoms- Patients with Wolff-Parkinson-White are often Asymptomatic
Palpitations
Dizziness
Syncope
What are the 4 ECG Features of Wolff-Parkinson-White Syndrome?
Delta Waves (Slurred Upstroke in the QRS)
Short PR Interval (<120ms)
Broad QRS
If a re-entrant circuit has developed, the ECG will show Narrow Complex Tachycardia
What 5 investigations can be ordered if Wolff-Parkinson-White Syndrome is suspected?
ECG
24 Hour ECG monitoring if Paroxysmal Symptoms
Routine bloods include TFTs if Non-Cardiac causes of Tachycardia are suspected
ECHO to assess Ventricular Function
Intracardiac Electrophysiological studies to map the Location of the Accessory Pathway
What is the 3 step management of Wolff-Parkinson-White?
Radiofrequency Ablation of the Accessory Pathway
Drug Treatment (Amiodarone or Sotalol) to avoid further tachyarrhythmias. These are contraindicated in Structural Heart Disease
Surgical (open heart) Ablation- rarely done and only done in Complex Cases
What is the management of Wolff-Parkinson-White Syndrome in Unstable Patients?
Unstable Patients (3) (Blood Pressure<90/60mmHg or with signs of Systemic Hypoperfusion or Fast Atrial Fibrillation) require Direct Current Cardioversion (DC Cardioversion)
What is the 4 step management of Wolff-Parkinson-White Syndrome in Stable Patients?
3 for Orthodromic, 2 for Antidromic
They are managed according to their Rhythm
- If they have an Orthodromic AV Reciprocating Tachycardia (Narrow QRS Complex with Short PR Interval), management is with Vagal Manoeuvres (Carotid Sinus Massage or Valsalva Manouevre). If this fails, then IV Adenosine should be Administered
- In Orthodromic AV Reciprocating Tachycardia, one limb of the aberrant circuit involves the AV node so slowing conduction through the AV Node helps to Terminate the Tachycardia
- In Antidromic AV Reciprocating Tachycardia (Wide QRS Complex), Atrial Fibrillation or Atrial Flutter, Intravenous Antiarrhythmics (such as Procainimide or Flecainide) help prevent Rapid Conduction through the Accessory Pathway
- DC Cardioversion may be used if the symptoms still persist
