Emergency Medicine and Critical Care COPY Flashcards
What is Tosardes de Pointes
Tosardes De pointes is a form of polymorphic wide complex Ventricular Tachycardia that occurs in patients with Prolonged QT interval
Can degenerate into Ventricular Fibrillation
Can cause significant haemodynamic compromise and death
What is the management of Tosardes de Pointes?
If stable Treat with IV magnesium Sulphate over 1-2 minutes and stop any causative medications
if unstable with haemodynamic compromise, DC cardioversion can be done
In recurrent TdP despite Magnesium sulphate and correction of reversible causes, IV isoprenaline infusion is indicated
What are the causes of Long QT syndrome?
Causes of Long QT can be remembered using the mnemonic TIIMMES
T - Toxins: Drugs including anti-arrhythmics, anti-psychotics and tricyclic antidepressants, macrolide antibiotics can also increase QT interval e.g erythromycin
I - Inherited: Congenital long QT syndromes such as Romano-Ward, Jervell, Lange-Nielson syndromes
I - Ischaemia
M - Myocarditis
M - Mitral Valve prolapse
E - Electrolyte abnormalities such as hypokalaemia and hypocalcaemia
S - Subarachnoid Haemorrhage
Why does Ondansetron increase QT interval?
Ondansetron is a 5HT3 antagonist - helps reduce nausea and for patients who can’t keep oral foods down - can increase QT interval and puts patients at risk of TDP
Methadone can prolong QT interval
Why can’t Cyclizine be prescribed to the elderly or IVDU?
Cyclizine is a H1 receptor antagonist and used for travel sickness
It has anti-cholinergic effects which can increase high from opiates especially methadone and avoided in the elderly cause it can lead to delirium
What is a Pulmonary Embolism?
A Pulmonary Embolism is a sudden blockage of a major blood vessel of the lung usually by a clot
How does Pulmonary Embolism present?
Presentation is variable but clinical features include:
- Pleuritic Chest pain
- Difficulty breathing
- Hypoxia
- Haemoptysis
- Low grade fever
- Syncope (only sometimes though)
Patients may also have signs of symptoms of a DVT affecting their limbs
What are the risk factors for Pulmonary Embolism?
Risk factors can be remembered using the mnemonic A EMBOLISM:
- A - Age
- E - Ex (previous) DVT/PE
- M - Malignancy
- B - Baby (Pregnancy)
- O - Oestrogen: OCT/HRT
- L - Large (Obesity)
- I - Immune conditions/Inherited Thrombophilias: such as anti-phospholipid syndrome, factor V Leiden
- M - Mobility: Surgery within the last 2 months, bed rest >5 days, recent air travel
What are the most common ECG findings in PE?
Sinus tachycardia (regular rhythm) is the most common finding
Right heart strain can also be seen - Right Bundle Branch Block, right axis deviation, T Wave inversion and ST segment changes
There is also the rare S1Q3T3 features (Large S wave in lead 1, Q wave and T wave inversion in lead 3)
What are the other investigations in PE?
Well’s Score should be calculated - if Well’s score is low, then D-dimer should be measured - if Well’s Score is high (with or without abnormal d-dimer level), a CTPA (CT Pulmonary angiogram) should be ordered
D-dimer levels are useful for it’s negative predictive value - causes of false positive d-dimer value includes pregnancy, old age, malignancy and infections
A CTPA is the gold standard investigation for a suspected PE
What is the acute management for PE?
Should be assessed using ABCDE
A - Airway: likely to be patent
B - Breathing: the patient may be tachypnoeic and hypoxic. Oxygen should be administered (i.e 15L of oxygen via non-rebreathe mask)
C - Circulation: Patient may be tachycardiac. Signs of right heart strain are suggestive of sub-massive PE. Hypotension is suggestive of a massive PE. Consider intravenous fluids if the systolic blood pressure is <90mmHg
D - Disability: likely to be unremarkable
E - Exposure: the patient may have a low grade pyrexia. Important to check for signs of DVT. consider analgesia at this stage if required
Thrombolysis (intravenous bolus of Alteplase) is indicated in massive PE. debate over whether it should be administered in a sub-massive PE.
Management should also include anticoagulation, with guidance currently suggesting a DOAC (Direct-acting oral anti-coagulant) as first-line
Patients showing evidence of right heart strain and persistent hypotension may be candidates for intra-arterial or intravenous thrombolysis
What is the Interventional management of PE?
Embolectomy may be considered in patients with massive PE when thrombolysis is contraindicated
What are the complications of PE?
- Obstructive shock
- Arrhythmias
- Pulmonsary artery hypertension
- Death
What is a tension pneumothroax?
Tension pneumothorax is where air is trapped in the pleural cavity under positive pressure, displacing the mediastinal structures and compromising cardiopulmonary function
TP occurs when air enters the pleural cavity through a one way valve and cannot escape.
Life threatening because it can lead to pressure of mediastinal organs if not treated immediately
What are the causes of Tension Pneumothorax?
Penetrating Trauma from road traffic accident or iatrogenic procedures such as central line insertion or lung biopsy
What are the clinical features of Tension Pneumothorax?
Clinical Features include:
- Haemodynamic instability: Tachypnia, tachycarida, hypotension, raised JVP
- Tracheal Deviation away from the affected side
- Decreased chest expansion
- Increased resonance on percussion
- Decreased breath sounds
- Decreased vocal resonance
- Surgical emphysema
TP is a clinical diagnosis and should be treated immediately
What are the signs on examination with a right sided tension pneumothorax
- Trachael deviation to the left
- Reduced chest expansion
- Hyper resonant on the right
- Decreased vocal resonance on the right
What is the management of Tension Pneumothorax?
Treatment involves immediate needle decompression with large bore needle inserted into the 2nd intercostal space in the midclavicular line just above the third rib (to avoid damaging the neurovascular bundle below that sits below each rib) - this is called needle thoracocentesis
Should then be followed by chest drain insertion to reduce the risk of an immediate recurrence of the TP
What is Supra-ventricular tachycardia?
Supraventricular tachycardia is any narrow complex tachycardia characterised by a heart rate of more than 100bp and a QRS width of less than 120ms on an ECG
What are the most common SVTs?
- Atrial Fibrillation
- AV re-entry Tachycardia (AVRT)
- AV Nodal Re-entry Tachycardia (AVNRT)
What are the features of AV Nodal Re-entry Tachycardia on ECG?
- Narrow Complex tachycardia
- P waves that occur after QRS (short PR interval) or are englufed by QRS (not visible)
What are the adverse features of SVT and management?
Remember Mnemonic HISS:
- H - Heart Failure
- I - Ischaemia
- S - Shock
- S - Syncope or hypotension (SBP <90mmHg)
Patients with adverse features should be given synchornised DC schock
What is the management of SVT in stable patients?
In stable patients, it depends on whether their rhythm is regular or irregular
if regular:
- vagal manoeuvres such as carotid sinus massages or the Valsalva manoeuvre
- If this fails then IV adenosine 6mg (works by temporarily blocking AV node - should also be warned that they might experience difficulty breathing, chest tightness or flushing)
- should be given rapidly over 1-3 seconds followed by a bolus of 20ml IV normal saline - if this fails a second dose of Adenosine 12mg can be administered and then followed by another 18mg
- If this fails then beta-blocker or Verapamil can be tried before DC cardioversion
- Should be noted that asthma is a major contraindication of Adenosine so if patient has history of asthma then give Verapamil instead after vasovagal maneuvores
If irregular rhythm, should be treated as AF according to algorithm
What is the management of SVT in unstable patients?
Synchronised DC cardioversion
What are the contraindications to the use of Adenosine?
IV adenosine 3mg should not be administered to heart transplant patients, those with Central line access or medications that can potentiate adenosine such as Dipyridamole or Carbamazepine
Asthma is a contraindicated to Adenosine so Verapamil should be used
What are the complications of AVT?
- Syncope
- DVT
- Embolism
- Cardiac Tamponade
- Congestive Heart failure
- Myocardial infarction
- Death
What is Ethylene Glycol Poisoning?
Ethylene glycol poisoning occurs when anti-freeze and can be ingested on purpose or accidently
What are the early features of Ethylene Glycol poisoning?
Early features are under 24 hours
- Apparent intoxication (like alcohol drunk)
- Nausea and vomiting
- Haematemesis
- Seizures
- Ataxia
- Opthalmoplegia
- Papilloedema
- Raised anion gap (metabolic acidosis)
- Pulmonary Oedema
What are the late features of Ethylene Glycol poisoning?
Late features are over 24 hours
- Acute tubilar necrosis
- Hypocalcaemia
- Hyperkalaemia
- Hypomagnesaemia
What is the management of Ethylene Glycol poisoning?
If under 1 hour since ingestion gastric lavage or NG aspiration
Fomepizole (acts as a competitive inhibitor of alcohol dehydrogenase) - prevents metabolism of EG into toxic metabolites
Alcohol (ethanol) can be used if fomepizole is unavailable
Haemofiltration can be used in severe cases
How do you manage pain in palliative patient?
Opioids are commonly administered subcutaneously
If patient has other symptoms such as nausea, vomiting, colicky pain and increased secretions - can be treated with:
- Hyoscine Butylbromide (muscarinic antagonist - first line)
- Octreotide
- Ondansetron (primarily used for nausea and vomiting in chemo patients - 5-HT3)
- Atropine
What are some of the common causes of Upper GI Bleeds
- Peptic Ulcers
- Portal Hypertension
- Variceal Bleeding
What is a peptic ulcer (Upper GI Bleed)
Peptic ulcers encompass both gastic and duodenal ulcers
What are the risk factors for peptic ulcers
- NSAIDS
- Smoking
- Alcohol
- H. Pylori infection
- Steroids
- Stress
How do peptic ulcers present?
Present with epigastric pain which occurs after food ingestion - will often have epigastric tenderness
Can be prominent at night
If on posterior wall, it may cause pain to radiate through to the back
If there is significant acute bleeding, there may be tachycardia and hypotension suggesting hypovolaemic state
Anecdotally, gastric ulcers can be differentiated from duodenal as in gastric, pain is worse right after eating but in duodenal pain worse several hours after eating - again VERY ANECDOTAL
How are peptic ulcers diagnosed?
Diagnosis is confirmed using oesophago-gastro-dudenoscopy (OGD)
What is portal Hypertension?
Portal hypertension describes elevated pressure in the portal venous system
What are the causes of portal hypertension?
Can be divided into three broad causes: Pre-hepatic, hepatic, post-hepatic
Pre-hepatic: obstructions of portal vein i.e portal vein thrombosis, extrinsic pressure from tumour
Hepatic: Cirrhosis, chronic hepatitis, schistosomiasis (parasitic worms)
Post-Hepatic: Due to obstructions of hepatic veins or venules i.e Budd-chiari syndrome (blood clot obstruction), right-heart failure
Most common cause is Cirrhosis
Where is the most common rupture within the portal vein system?
the most common place is the gastro-oesophageal junction as those walls are the thinnest
How does Variceal bleeding present?
Presents with features of upper GI bleed:
- Haematemsis
- abdominal pain
- Malaena (black tarry stool
- features of liver disease due to portal hypertension
- if bleeding significant, tachychardia, hypotension suggesting a hypovolaemic state
How do we categorise patients into risk groups for Upper Gi bleed
Prior to endoscopy - Glasgow-blatchford scale - any score greater than 0 suggests high risk GI bleed
Post endoscopy - Rockall Score - used to estimate risk of rebleeding and risk of mortality
What are the investigations for Upper GI Bleed?
- Glasgow-Blatchford score
- Routine bloods
- Clotting
- Group and save
- Cross-match
What is the treatment of any Upper GI bleed?
- ABCDE assessment
- Insert 2 large bore IV cannulae and take bloods for FBC, U+E, LFT, clotting, cross match (check blood antibodies)
- IV fluids - fluid challenge if hypotensive
- Catheterise
- Correct clotting if needed
- Urgent endoscopy
What is the management of Non-Variceal bleeds (i.e ulcers)?
Endoscopy is first line for bleeding from ulcer - i.e active bleeding lesions, non bleeding visible vessels or ulcers with adherent blood clot
theraputic measures include, clipping, thermal coagulation, fibrin or thrombin - adrenaline injection can be given but adjunctively only
Oozing ulcers should be left alone as they have good prognosis without intervention
Interventional radiology should be considered for unstable patients who re-bleed after initial endoscopic treatment. Percutaneous angiography can be used to identify point of bleeding which can then be embolised
Drugs for acid suppression should not be offered prior to endoscopy - proton pump inhibitors should be given when evidence of non-V Upper GI bleed and recent bleeding seen in endoscopy
What is the management of acute Variceal Bleeding?
Terlipressin is used in suspected variceal bleeding and acts as a vasopressin analogue - should be stopped after haemostasis or after 5 days
Prophylactic antibiotics such as Tazocin should also be given in suspected variceal bleeding
Oesophagogastroduodenoscopy can also isolate and treat the cause of the variceal bleeding
Endoscopic haemostatic measures for bleeding varices include band ligation and injection of N-butyl-2-cyanoacrylate
The formation of a transjugular intrahepatic portosystemic shunt (TIPS) should be considered if all else fails to control the bleeding
What is Horner’s Syndrome?
Horner’s Syndrome is characterised by ptosis, meiosis with or without anhydrosis.
It is due to an interruption of the sympathetic nerve supply to the eye and can be classified into pre-ganglion causes, post ganglionic causes and central causes
What are the causes of horner’s syndrome?
Pancoast tumour (affecting sympathetic nerve supply - presents as ipsilateral horner’s syndrome with thoracic outlet syndrome) - an invasive apical lung cancer invading the sympathetic plexus and brachial plexus - can cause a hoarse voice and bovine cough if affecting laryngeal nerve
Stroke
Carotid artery dissection (Red flag: neck pain)
Lateral Medullary syndrome - but would present with more symptoms such as ipsilateral vestibular nuclei deficits (nystagmus, vertigo, vomiting) and ipsilateral cerebellar signs (ataxia)
What is the emergency management of head trauma?
need to be assessed - ABCDE with focus on stabilising c-spine and airway, recognising haemorrhage and treating pain
If decreased GCS, alcohol excess and a history of a fall - could be risk factors of subdural haematoma so get urgent CT head
In paeds patients, take a note of the weight of the child
What is Pulmonary Oedema?
Pulmonary oedema is a condition caused by excess fluid in the lungs
How does acute pulmonary oedema present?
Presents with extreme dyspnea, restlessness and anxiety
Some patients may produce pink and frothy sputum
They may have signs of fluid overload:
- Bilateral reduced air entry and inspiratory crepitations
- Raised JVP
- S3 gallop - a third heart sound that occurs right after S2
- Peripheral Oedema
What can lead to acute pulmonary oedema?
- Cardiac Ischaemia
- Arrhythmias
- Non-compliance with regular heart failure medication
What are the investigations for acute PO?
- ABG
- ECG
- Troponin if concerned about a new cardiac event
- Serum BNP
- Chest X-ray
- Bedside observations
What is the management of acute PO?
- ABCDE
- Sit the patient up
- Adminster Oxygen
- Ensure IV access
- IV Furosemide (40mg IV)
- Consider non-invasive ventilation such as CPAP if medical therapy failed
- In ICU/ITU setting consider invasive ventilation and inotropic support (IV dobutamine or Milrinone - especially if patient has severly reduced LV systolic function i.e low ejection fraction) if all of above fails
Morphine can be given to patients who are very anxious and in severe respiratory distress - give with metoclopramide (an antiemetic) to offset the nausea and vomiting side effects of morphine
What is the management of patients with Heart failure and renal impairment with PO?
AKI is normally pre-renal due to under-perfusion and can be managed by replacing fluid as patients are normally hypovolaemic
In cases of heart failure + AKI, the underperfusion is however due to poor output from the heart and patients have fluid overload (the left ventricle end diastolic volume is too high so stroke volume falls)
So in these patients off-loading fluid with diuresis results in improved stroke volume and so greater output from heart and improved kidney perfusion - so diuresis can also recover renal function
What is the management of PO in patients with heart failure with hypotension?
Difficult to manage as diuretic can further lower BP and impact perfusion of vital organs - if patients has low LV ejection fraction and systolic below <85mmHg or patient is shocked (cool extremities, confusion) - then addition of inotrope may be indicated but discuss with senior - In interim give 250ml boluses over 15-20 mins to keep blood pressure above 90mmHg but need careful titration
Vasopressors like noradrenaline can also be added when there is persistent hypotension + end-organ hypoperfusion - but only after insufficient response to inotropes
All these measures are temporary tho and just used to maintain until the acute trigger for the deterioration has been reversed
What is the presentation 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 (due to wasting of bicarbonate ions due to ingested acid load) - can be mixed with resp alkalosis
How is diagnosis of aspirin overdose made?
- VBG - looking for acid-base imbalance
- Measure Salicylate levels
How is Aspirin Overdose managed?
If ingestion <1 hour ago - then use activated charcoal
Otherwise IV fluid, sodium bicarbonate and potassium chloride - this alkalises the urine in order to increase salicylate excretion and should be monitored with VBGs
Dialysis may be necessary if blood levels are extremely high
Monitor for complications by checking Renal function - get chest x-ray for pulmonary oedema and CT head if signs of cerebral oedema
What is Diabetic Ketoacidosis?
DKA is a life-threatening complication of diabetes characterised by hyperglycaemia, hyperketonaemia and metabolic acidosis - there is partial respiratory compensation
How do you make a diagnosis of DKA?
- Capillary blood glucose (>11mmol/L)
- Capillary blood ketones (>3mmol/L)
- Venous blood gas - for bicarbonate (<15mmol/L) and pH(<7.3)
- Urine dip (Ketones 2+ or more)
You will expect to find low or normal sodium in DKA
How do we find the causes/complications of DKA?
- U+Es - looking for electrolyte abnormalities
- FBC - looking for raised infective markers
- Blood cultures
- Urine MSU
- Chest X-ray - looking for focus of infection
- ECG - complications of potassium disturbance
The common precipitants of DKA include infection, trauma and myocardial infarction
What are the clinical features of DKA?
- Abdominal pain
- Vomiting
- Lethargy
- Dehydration - may lead to hypotensive (also from acidosis effects) → coma and death
What are the complications of DKA?
- Pre-renal kidney failure - secondary to dehydration
- Hyperkalaemia - may be secondary to pre-renal failure (so not reccommended to give potassium in the first bag of fluids)
- Hypokalaemia - secondary to kidney loss during diuresis and shifts into cells following insulin infusion
- Hypoglycaemia - As a consequence of rapid correction of ketosis
- Cerebral oedema - rare in adults - may be caused by rapid fluid shifts during rehydration
- Pulmonary Oedema - secondary to rapid rehydration
- Rhabdomyolysis
- Thrombosis
- Stroke
What are the principles of treatment for DKA?
Initial treatment of DKA involves fluid resuscitation and maintenance as patients can be severely dehydrated
Hyperglycaemia and acidosis can be corrected with insulin treatment
When plasma glucose drops below 11.1mmol/L, 5% dextrose should be added to IV fluids - Electrolyte abnormalities like hypokalaemia should be corrected
How do you manage DKA?
Management of DKA is time dependent and in paeds, fluids resus more cautious due to risk of Cerebral Oedema but in adults the following:
In hour 1:
- 1L 0.9% Saline over 1 hour
- Give STAT fluid challenge if systolic under 90
- Fixed rate insulin infusion (0.1 units/kg/hr i.e 50 units Actrapid in 50mL 09% saline) AFTER commencing fluids
- Continue any long acting insulin patient is on
- check blood glucose, ketones and GCS every hour
- Continuous ECG monitoring
In hours 2-12:
- Continue fluid resuscitation (with potassium if serum K<5.5mmol/L - check before every bag
- 1L 0.9% saline + 40mmol KCl over 2 hours, then 2 hours again then over 4 hours then over 4 hours again then over 6 hours
- Make sure ketones are falling at least 0.5mmol/L/Hour if not then increase insulin rate
- Consider catheter to measure urine output at for at least 0.5ml/kg/hour
- if cap glucose drops below 14mmol/L start 125ml/hour 10% glucose alongside the saline
- continue fixed rate insulin until Blood ketones <0.3mmol/L and ph>7.3 and bicarbonate >18mmol/L
In hours 12-24:
- Aim for normal biochemical parameters
- if patient unable to eat and drink then start sliding scale insulin
- if able to eat and drink then restart subcutaneous insulin regimen - will need some crossover with IV insulin
What GCS score suggests that patient is unable to maintain their own Airway?
8
What is Glandular Fever?
A.K.A Infectious mononucleosis is a viral infection caused by EBV and transmitted through saliva
How does Glandular fever present?
Mild infection in small children but a severe infection in teenagers - with fatigue persisting for a few weeks
How is a diagnosis of EBV infection made?
Usually made clinically - but heterophile antibody ‘Paul Bunnell’ test will be positive if performed
What is the management of Glandular Fever?
Management is supportive - acute EBV can cause hepatomegaly and splenomegaly - splenomegaly can be so large and high risk of rupture that patients are recommended to avoid heavy lifting or contact sports for 1 month
Why should amoxicillin be prescribed in cases of bacterial pharyngitis where glandular fever is suspected?
Should never prescribe amoxicillin for bacterial pharyngitis if glandular fever is suspected as it can cause a widespread rash until amoxicillin is stopped and supportive management initated
What is acute coronary syndrome?
Umbrella term covering STEMI, NSTEMI and unstable angina
What is unstable angina?
Unstable angina is a critical narrowing of coronary artery causing ischaemia
- Characterised by chest pain at rest or minimal exertion lasting >15 minutes
- ECG changes (new ST depression or T wave inversion
- NO rise in troponin; no myocardial necrosis
What is a NSTEMI?
NSTEMI is a partially occluded coronary artery
- Characterised by chest pain at rest or minimal exertion lasting >15 minutes
- ECG changes (new ST depression or T wave inversion
- Rise in troponin; myocardial necrosis
Can differentiate between NSTEMI and unstable angina by a rise of troponin in NSTEMI
What is a STEMI?
A STEMI is a completely occluded coronary artery
- Characterised by chest pain at rest or minimal exertion lasting >15 minutes
- ECG changes (New ST-elevation or left bundle branch block)
- Rise in troponin; no myocardial necrosis
NSTEMI and STEMI are differentiated by the ECG findings
How do you diagnose a STEMI?
To diagnose STEMI, there needs to be new ST elevation in 2 or more contiguous leads. must be larger than or equal to 2mm in precordial leads or more than or equal to 1mm in the limb leads
What is the single best initial management for ACSs?
Remember the Mnemonic MMONAC
- M - Morphine
- M - Metoclopramide
- O - Oxygen (if Sats <94%)
- N - Nitrates (GTN spray) - if patient has systolic below 90mmHg then the use of GTN spray is contraindicated as GTN can cause a decrease in blood pressure - this cut off should be used in the clinical context
- Asprin 300mg PO
- Clopidogrel 300mg
What is the treatment of a STEMI?
- PCI can be considered if patient presents within 12 hours of symptom onset and within 2 hours of medical contact - they should be haemodynamically stable
- if patient within 12 hours of onset but after 2 hours of medical contact, offer thrombolysis - provided they are stable and have no contraindications - if contraindicated to thrombolysis PCI can be done
- if patient presents more than 12 hours of symptom onset, pharmacotherapy should be management of choice if they are asymptomatic and stable - otherwise revascularization can be considered
What are the contraindications to thrombolysis in MI?
AGAINST
- A - Aortic Dissection
- G - GI Bleed
- A - Allergic Reaction
- I - Iatrogenic: recent surgery
- N - Neurological disease: recent stroke (within 3 months), malignancy
- S - Severe hypertension (>200/120)
- T - Trauma, including CPR
What is the treatment of a NSTEMI?
start MMONAC then stratify the patients according to either the TIMI score or GRACE model depending on the hospital
patients at high risk of death and further ischaemic events should be offered re-vascularisation within 12-24 hours - patients found to be at low risk can be managed conservatively with medications
They can be discharged after having stabilised and should have further cardiac investigations in the future
What is Status Epilepticus?
Status Epilepticus describes any seizure activity that lasts more than 5 mins or if the patients experiences more than one seizure + does not fully regain consciousness between the two
What is the management for Status Epilepticus?
- ABCDE
- Oxygen
- Ensure IV access
- Arterial blood gas
- take bloods for glucose, FBC, UE, CRIP, Calcium, Phosphate, Magnesium, drug levels if patient on anti-epileptic medications
- Need anaesthetic review to ensure the airway is managed
- Give IV Lorazepam 4mg - followed by second dose if no response - If IV access not gained, first line is then administration of PR Diazepam or Buccal Midazolam
- If initial benzodiazepines fail, further anticonvulsants can be used (Leviteracetam, Phenytoin, Valproate)
- If seizures carry on then persist, intubate and general anesthesia is necessary
What is Rapid Sequence Induction?
Rapid Sequence Induction is a method of coordinating the administration of rapidly acting induction agents to produce anaesthesia and muscle relaxation followed by prompt intubation resulting in a secure airway with minimal risk of aspiration
What are the specific pre-defined roles for healthcare staff?
- Airway
- Drug Preparation
- Monitoring of Vital signs
- Drug administration
- Cricoid pressure
What are the steps to forming the sequence of RSI?
Think the 7 Ps:
- P - Preparation - make sure environment is optimised
- P - Pre-oxygenation - administer high flow oxygen for 5 minutes prior to procedure
- P - Pretreatment - may involve administration of opiate analgesia or fluid bolus to counteract the hypotensive effect of anaesthesia
- P - Paralysis - administration of the induction agent e.g propofol or Sodium Thiopentone and a paralysing agent e.g Suxamethonium or Rocuronium
- P - Protection and positioning - cricoid pressure should be applied to protect the airway following paralysis - in line stabilisation may be required in some cases
- P - Placement and proof - Intubation is performed via laryngoscopy with proof obtained (direct vision, end tidal CO2, bilateral auscultation)
- P - Post-Intubation management - taping or tying the endotracheal tube, initiating mechanical ventilation and sedation agents
How does Digoxin poisoning present?
- Dizziness
- Nausea and vomiting
- Palpitations (due to arrhythmias)
- Bardycardia typically without hypotension
- Yellow-green colour disturbance
- Visual halos
- Confusion
- Hyperkalemia (hypokalemia is a risk factor for toxicity)
How do you manage digoxin poisoning?
- Immediate Digoxin level
- IV fluids
- Correct electrolyte abnormalities
- Continuous cardiac monitoring
- Give digiband if level >15ng/mol after 6 hours of last dose OR level >10ng/ml within 6 hours of last dose OR symptomatic
What is McBurney’s Sign?
McBurney’s Sign can be located one-third of the distance from the anterior superior Iliac spine to the umbilicus on the right side and tenderness there indicates acute appendicitis - other signs of appendicitis are Rovsing’s sign (palpatiation of left lower quadrant elicits pain in the right lower quadrant) and Psoas sign (right lower quadrant pain elicited on stretching of the iliopsoas muscle)
What is Epistaxis?
Epistaxes are nosebleeds and can vary from minor bleeds to life-threatening haemorrhages requiring hospitalisation and surgical treatment
what are the causes of epistaxes?
They can be primary or secondary
the majority of primary where there is no clear or obvious cause
Secondary epistaxis causes can be:
- Alcohol
- Antiplatlet agents (e.g clopidogrel)
- Asprin and NSAIDS
- Anticoagulants (e.g warfarin)
- Coagulopathy (e.g haemophilia, Von Willebrand’s Disease)
- Trauma (e.g Nasal Fracture)
- Tumours
- Surgery
- Septal perforation
What is the management of Epistaxis?
- ABCDE
- Take brief history
- First line is direct compression for 10-15 minutes → if it doesn’t work and the epistaxis is an anterior position then move onto cauterisation (done through 75% silver nitrate sticks applied to the bleeding site for 3-10 seconds + anaesthesia through lidocaine with phenylephrine) - if posterior or bleeding point not identified, severe bleeding move straight to nasal packing → nasal packing through nasal tampons inflateable packs or ribbon gauze impregnated with vaseline can be used
- More aggresive therapies include nasal balloon catheres and transnasal endoscopy with direct cautery/arterial ligation are for posterior bleeds and patients unamenable to nasal packing
How do you increase pain medication?
Increase current dose by ⅓ i.e 90mg to 120mg and control breakthrough pain with oramorph with 1/6 mg of total MST dose PRN i.e if total dose is 120mg then give 20mg prn of oramorph to control breakthrough pain
How do we classify the cuases of Pneumothroax?
- Can be classified as either spontaneous and traumatic
- Spontaneous can be due to either primary causes or secondary causes - primary causes mean that there is no underlying pathology and secondary causes means there are
- Traumatic can either be due to iatrogenic causes e.g insertion of central line or positive pressure ventilation or non-iatrogenic causes e.g penetrating trauma or blunt trauma with rib fracture
What are the spontaneous secondary causes of pneumothorax?
- Connective tissue disorders e.g marfan’s syndrome and Ehlers-Danlos syndrome
- Obstructive lung disease e.g asthma and COPD
- Infective lung disease e.g TB and Pneumonia
- Fibrotic lung disease e.g cystic fibrosis and idiopathic pulmonary fibrosis
- Neoplastic lung disease e.g Bronchial carcinoma
What is the management of simple primary pneumothorax?
- If patient is NOT short of breath AND the pneumothorax is <2cm on x-ray -conservative management is enough and patient should be discharged and reviewed in 2-4 weeks
- if patient is short of breath OR pneumothorax is >2cm, patient should be aspirated with 16-18G cannula under local anaesthetic - if this fails patient an intercostal drain is necessary
What is the management of simple secondary pneumothorax?
- if patient is NOT short of breath AND pneumothorax is <1cm, does not require any further invasive intervention but should be admitted for observation for 24 hours and administer oxygen as required
- If patient is NOT short of breath and the pneumothorax is 1-2cm on x-ray, aspiration is required, if successful the patient can be admitted for 24 hours of observation - if unsuccessful, the intercostal drain is necessary
- if patient IS short of breath OR pneumothorax is >2cm on x-ray, an intercostal drain is necessary
How do you manage a Paracetamol Overdose?
Management is dependent both on how paracetamol was taken and when - treatment based on nomogram i.e if paracetamol levels above treatment line then start NAC
- If ingestion under an hour + dose >150mg/kg - give activated charcoal
- If staggered dose or ingestion >15 hours ago: Start N-acetylcysteine immediately
- if ingestion <4 hours ago: Wait until 4 hours to take a level and then treat N-acetylcysteine based on level
- If ingestion 4-15 hours ago: Take immediate level and treat based on level
- If patient presents after 16 hours/uncertainty about timing/has staggered overdose then give NAC immediately
Obtain following bloods:
- FBC
- Urea and Electrolytes
- INR
- Venous gas
If bloods worsening then transfer to liver unit
What are the clinical features of Benzo overdose?
- Lethargy
- Ataxia
- Slurred speech
- Coma
- Respiratory Distress
What are the clinical features of Beta-block overdose?
- Bradycardia
- Hypotension
- Mild Hypoglycaemia
- Mild Hyperkalemia
What are the clinical features of Opiate overdose?
- Confusion
- Pinpoint pupils
- Respiratory distress
- Cyanosis if severe
What are the clinical features of Phenothiazine overdose?
- Dystonia
- Sedation
- Dry mouth
- Hyperthermia
- Dysrhythmias
What are the clinical features of organophosphate overdose?
- Salivation
- Lacrimation
- Urination
- Diarrhoea
- Small pupils
- Fasciculations
- Bradycardia
What are the clinical features of MDMA overdose?
- Agitation
- Tachycardia
- Hyperthermia
- Acute Renal Failure
- Hypo/hypertension
- Mydriasis (dilated pupils)
What are the clinical features of Cocaine overdose?
- Anxiety
- Agitation
- Aggression
- Paranoid Psychosis
- Hyperthermia
- Seizures
- Arrythmias are also possible and if untreated will lead to cardiac arrest
What is the management of Pulseless electrical activity and Asystole?
These are non-shockable rhythms - so CPR should be commenced immediately
Adrenaline 1mg IV should be given in first cycle of CPR and should it still be non shockable then should be administered every other cycle
What is Ventricular Fibrillation and Pulseless Ventricular Tachycardia?
VT is a regular broad complex tachycardia
VF presents as chaotic irregular deflections of varying amplitude
They are both shockable rhythms
What is the management of VF and pulseless VT?
Defib + CPR is mainstay
Non-synchronised DC cardio version should be used in patient with VT/VF - after the first shock CPR should carry on for a further 2 minutes
if still persistent then amiodrone 300mg IV and adrenaline 1mg IV (1:10,000) should be given after third shock is delivered - adrenaline should be repeated every other cycle
How does Acute pancreatitis lead to Tosardes de Pointes?
Acute pancreatitis causes hypocalcaemia which prolongs the QT interval and therefore can lead to TdP
What is the management of Hypoglycaemia?
When mild (i.e still conscious):
- Eat/drink 15-20g fast acting carbohydrates such as glucose tablets, small can of cocacola, sweets or fruit juice
- Avoid chocolate
- Eat some slower acting carbohydrates afterwards (e.g toast)
If severe (e.g unconsious, seizing):
- 200ml 10% dextrose IV (can also be given as 100ml 20% glucose IV)
- 1mg/kg glucagon IM if no IV access (will not work if caused by acute alcohol because of its action in blocking gluconeogenesis)
- Treat siezure if prolonged or repeated
What is Oesophagitis?
Oesophagitis is an inflammation of the lining of the gullet commonly caused by the reflux of gastric contents into oesophagus
Can also be caused by drugs (e.g Doxycycline - due to its direct chemical irritant effect on the mucosa), infection and allergens (e.g eosinophilic oesophagitis)
What are the symptoms of Oesophagitis?
- Heartburn (retrosternal burning pain)
- Nausea +/- vomiting
- Odynophagia (painful swallowing)
What are the investigations for Oesophagitis?
Endoscopy allows direct visualisation of oesophagus and can be used to grade the degree of Oesophagitis (Savary-miller grading system or Los Angeles grading system) - biopsy can be taken at the same time as endoscopy
If reflux is suspected then oesophageal pH monitoring to identify the timing of symptoms and reflux correlate
What is the management of Oesophagitis?
managed conservatively through lifestyle changes i.e weight loss, stop smoking, reduced alcohol intake
Pharmacological treatements include trial of full dose proton pump inhibitors for one month
What is Fast Atrial Fibrillation?
Atrial fibrillation occurs when abnormal electircal impuselses suddenly start firing in the atria - overriding the AVN causing a highly irregular pulse rate - if heart rate is >100bmp it is defined as FAst
On ECG you would see irregular QRS complex with absent P waves
What is the management of AF?
Depends on a number of factors:
- Presence of adverse sings
- Duration
- Likelihood of successful cardioversion (e.g age, previous attempts, known reversible precipitatnt)
Adverse signs are:
- Shock
- Syncope
- Heart failure
- Myocardial Ischaemia
The presence of any of these signs in the context of tachycardia is an indication for DC cardioversion
If these signs are absent - an AF with a duration <48 hours can be safetly cardioverted - those with unkown duration or duration >48 hours require anticoagulation for a minimum of 3 weeks before and 4 weeks after cardioversion due to risk of stroke from left atrial appendage thrombus.
Patients who are not cardioverted require life long anti-coag based on their CHA2DS2 VaScscore
What are the causes of post-operative nausea and vomiting?
- Infection
- Hypovolaemia
- Pain
- Paralytic ileus
- Drugs
How do we manage post-operative nausea?
in order to prevent post-operative nausea and vomiting, multi-modal alagesia model reccommended where anti-emetics of different mechanisms are used in combination for their synergistic effects
there are non-pharmological managements:
- Minimise patient movement
- Analgesia
- IV fluids if dehydrated
Pharmalogical management:
- 5HT3 receptor antagonists e.g ondansetron - which is first line but has risk of QT prolongation and constipation
- Histamine (H1) receptor antagonist e.g. Cyclizine. avoid in severe heart failure
- Dopamine (D2) receptor antagonist e.g. prochlorperazine. risk of extrapyramidal side effects (dystonic reaction)
- Corticosteroids or Metoclopramide (avoid in bowel surgery as can percipitate bowel obstruction) reserved for specific cases of post operative nausea and vomiting
for example if patient recieved cyclazine intraoperatively, prescribe ondansteron 8mg IV (give IV if patient vomiting as PO won’t work) post op for synergistic effect
What factors in AKI indicate referral for haemofiltration (dialysis) in ICU?
Think AEIOU BLAST
- A - Acidosis (ph <7.2 or bicarbonate <10mmol/L)
- E - Electrolyte (persistent hyperkalemia i.e >7mmol/L)
- I - Intoxication - overdose of Barbiturates Lithium Alcohol Salicylates Theophylline
- Oedema (pulmonary that is refratory)
- Uraemia (urea >40 or symptomatic/complications e.g encephalitis, pericarditis)
What is AKI?
AKi is defined as increase in serum creatinine of 26 micromol/L within 48 hours or an increase in serum creatinine >1.5 times above baseline value within 1 week or urine output of <0.5 ml/kg/hr for > 6 consecutive hours
How do you manage Acute Kidney Injury?
- Find and treat causes (e.g Sepsis, drugs, obstruction)
- Bloods - FBC, U+Es, CRP, antibody screen if autoimmune causes suspected
- Urine Dip and Microscopy
- Bladder scan - if retention suspected
- Ultrasound renal tract - if obstruction suspected
- ECG - looking for hyperkalemia/pericarditis
- Stop renotoxic drugs
- ACE-I/ARBs
- Spironolactone
- Diuretics
- Gentamicin - may need dose adjustments if necessary for treatment
- NSAIDs
- Give IV fluid - aggresiveness depends on severity of AKI and comorbities
- Treat complications (e.g hyperkalaemia, acidosis)
- Give dialysis if:
- Persistently high potassium that is refractory to medical treatment
- Severe acidosis (pH<7.2)
- Refractory pulmonary oedema (does not respond to dietry sodium restriction and combined diuretic treatment)
- Symptomatic uraemia (pericaditis, encephalopathy)
- Drug Overdose (e.g aspirin)
What are the complications of AKI?
- Hyperkalaemia
- Pulmonary Oedema
- Metabolic acidosis leading to nausea, vomiting and drowsiness
- Chronic kidney disease
- Death
What are the ECG changes in Posterior STEMI
In Posterior STEMI, you would see reciprocal changes in leads V1-3 (ST depression, Broad R waves and upright T waves
In leads V7-9 you would see the opposite as it shows the posterior aspect of the heart
What are the ECG changes in PE?
- Sinus Tachycardia
- T wave inversion in leads V1-4
What are the ECG changes in Pericarditis?
- Global Saddle shaped ST elevation (concave shaped) seen in all leads
- PR depression
- T wave changes
Get an ESR and CRP test to confirm pericarditis
What are the signs of shock after surgery?
- Tachycardia and hypotension
- FBC, U+Es, CRP and culture should be sent off immediately
- Fluid bolus of crystalloid should be given in any patient showing hypovolemic shock
How does simple alcohol withdrawal present (6-12 hours after last drink)?
- Insomnia
- Tremor
- Anxiety
- Agitation
- Nausea and Vomiting
- Sweating
- Palpitations
How does alcohol hallucinosis present? (12-24 hours post drink)
- Hallucinations of visual, tactile or auditory origin
How does delirium Tremens present?
- Delusions
- Confusion
- Seizures
- Tachycardia
- Hypertension
- Hyperthermia
What are the indications for inpatient withdrawal?
- Patient drinking >30units a day
- Scoring over 30 on the SADQ score
- High risk of alcohol withdrawal seizures
- Concurrent withdrawal from benzos
- Signficant medical or psychiatric comorbidity
- Vulnerable patients
- Patients under 18
How do you manage alcohol withdrawal?
Assisted alcohol withdrawal required in patients who drink over 15 units per day or score over 20 in AUDIT questionnaire
- Chlordiazepoxide prescribed in a reducing regimen in accordance with the CIWA-Ar score and local protocol
- For alcohol-withdrawal seizures, patient should be prescribed a rapid-acting benzodiazepine (e.g IV lorazepam) - if agitated should also prescribe benzo
- Pabrinex (1 pair of ampoules once daily to prevent Wernicke’s encephalopathy) - if there are signs of Wernicks (confusion, ataxia, ophthalmoplegia or nystagmus) patients should be prescribed 2 pairs of ampoules TDS
- In delirium tremens offer oral lorazepam as first line, if symptoms persist or declines offer parenteral lorazepam
What is an NAC anaphylactoid reaction?
In an anaphylactoid reaction, immune mediators are released as a direct consequence of the drug itself - the appropraite management is to stop the infusion and to give 10mg IV chlorphenamine and restart the infusion at a slower rate once the symptoms settle
If patient is also wheezy due to reaction then salbutamol nebulisers can be considered
What are some of the signs of an opportunistic infection secondary to HIV?
- Seborrheic dermatitis during intercurrent illness
- Oropharyngeal candidiasis
What are the causes of Encephalitis?
- Most common cause of infectious encephalitis is Herpes Simplex Virus
- Cytomegalovirus (CMV)
- Adenovirus, Influenzavirus
- Tuberculosis
- Listeria
- Fungal: cryptococcosis, coccidiomycosis, histoplasmosis
- Tick borne encephalitis
How does Encephalitis present?
- Fever
- Headache
- Altered mental status
- Personality change
- Focal neurological defecits
- Convulsions
- HSV1 encephalitis is associated with temporal lobe involvement → olfactory seizures e.g foul smell of rotten eggs
How is a diagnosis of Encephalitis reached?
- CT may show medial temporal and inferior frontal lobe involvement with the presence of petechial haemorrhages in HSV encephalitis
- Lumbar puncture with CSF analysis - microscopy, serology, cultures
What is the treatment for Encephalitis?
Empirical treatment for suspected encephalitis includes IV aciclovir and IV ceftriaxone/cefotaxime
What is the acute management of a seizure?
Lorazepam 4mg IV
What is the most appropriate management for fast AF?
If patient over 65 and more than 48 hours after onset of symptoms - rate control is preferred to rhythm control - rate control options include beta-blockers, non dihydropyridine calcium channel block (rate limiting CA blockers like e.g diltiazem or verapamil) or digoxin - check for brittle asthma as betablockers are contraindiated in those patients
Rhythm control drugs like Flecainide, amiodarone (reserved for older more sedentary patients) and sotalol preferred in younger patients - but not in those with sturctural heart diseases
What are the features of moderate asthama?
- Increasing symptoms
- PEF >50-75%
- No features of severe asthma
What are the features of severe asthma?
- PEF 33-50%
- RR more than equals to 25
- HR more than equals to 110
- Inability to complete sentences in one breath
What are the features of life threatening asthma?
Remember 33,92,CHEST
- PEF <33%
- SO2 <92% or PO2<8
- Cyanosis
- Hypotension
- Exhaustion, altered counsiousness
- Silent Chest (feeble respiratory effort)
- Tachyarrhythmias
Patients with life threatening asthma can have a normal PCO2 between 4.6-6.0 - raised PCO2 is indication of near fatal asthma
When should asthma patient be admitted to critical care?
- Requiring ventilatory support
- with acute severe or life threatening asthma who is failing to respond to therapy as evidenced by
- Deteriorating peak flow reading
- Persisting or worsening hypoxia
- Hypercapnia
- Exhaustion, feeble respiration
- Respiratory arrest
What is the management of Asthma?
Immediate:
- Sit-up
- 100% O2 via non-rebreathe mask (aim for 94-98%)
- Nebulised Salbutamol (5mg) and ipratropium (0.5mg)
- Hydrocortisone 100mg IV or prednisolone 50mg PO
If life threatening:
- Inform intensive care team
- Mangesium sulphate 2g IV over 20 minutes
- Nebulised salbutamol every 15 minutes
If no improvement:
- Nebulised salbutamol every 15min
- Continue ipratropium 0.5mg 4-6hrly
- Consider aminophylline unless already on theophylline (this is no longer routinely done)
- ITU transfer for invasive ventilation
Monitor through
- Peak flow measurements every 15-30 min pre and post salbutamol
- SpO2 keep >92%
- Consecutive aterial blood gas measurements
How does pericarditis present?
- Sharp pleuritic chest pain that is relieved by leaning forward - may have had flu like prodrome recently
- Examination unremarkable except pericardial friction rub
- ECG may show PR depression and global saddle shaped ST elevation
- Troponin mildly elevated
What is the acute management of pericarditis?
- NSAIDS such as aspirin, ibuprofen, and naproxen
- Bed rest
- Colchicine and steroid may also be used
What is sepsis?
A clinical syndrome presenting with complications of the body’s response to infection
Sepsis is when SIRS + presumed/confirmed infection
What is Systemic inflammatory response syndrome?
2 or more of the following:
- >38C or <36C
- Heart rate >90
- Respiratory rate >20
- WBC >12000/mm3 or <4000/mm3
What is severe sepsis?
Sepsis + evidence of organ dysfucntion: confusion, hypoxia, oliguria, metabolic acidosis
What is septic shock?
Severe sepsis + hypotension, despite adequate fluid resus or lactic acidosis (lactate >4mmol/L)
What is the clinical presentation and observations of Septic Shock?
- Fever, sweats or chills
- Breathlessness
- Headache
- Nausea and Vomiting
- Diarrhoea
Observations:
- Tachycardia
- Hypotension
- Pyrexia
- Peripherally vasodilated
- Hypoxia
- Tachypnoea
What are the things to do in Sepsis?
- ABC Firstly
- Sepsis 6
- Take Bloods (FBC, U&E, LFT, CRP, Lactate, clotting)
- Take Blood Cultures
- Administer Oxygen if required (should be for all sepsis patients regardless of saturation - or below 94%)
- Administer broad specturm IV antibiotics
- Administer IV fluid resuscitation (crystalloid) - if systolic BP <90mmHg or lactate >4mmol/L
- Monitor Urine output - catheterise
Ongoing managment is IV antibiotic therapy, surgical removal of infection source, critical care involvement
What other investigations beyond spesis 6 should you do?
- Imaging e.g chest x-ray, echocardiogram, abdominal ultrasound
- Viral PCR
- Urinalysis +/- culture
- Lumbar puncture
If first endoscopy with therapeutic intervention for upper GI bleed fails what should you do?
Repeat endoscopy with therapeutic intervention - but attempt a different treatment than the first as long as patient haemodynamically stable
What are the stages of shock?
Stage 1 - Anxiety from patient
Stage 2 - Agitation and tachyardia
Stage 3 - Confusion, Tachycardia, Hypotension, Tachypnoea and reduced pulse pressure
Stage 4 - Heart rate >140 and unconsious
What are the normal vital signs in paediatric patients
Also any slight temperature should be a cause for concern as neonates and infants may not be able to generate true pyrexia
What are the commonly used fluids?
What is the GCS scoring scale?
How is a diagnosis of Extradural haemorrhage made?
- CT Head
- Will show up as bi-convex (lentiform) shaped haemotamoa which is hyperdense
What is the most common sign of epiglottitis on an X-ray?
The classic thumb sign on a lateral C-spine radiograph - represents an enlarged and oedematous epiglottis
Remember that
What is the triangle of safety for insertion of a chest drain?
The space bounded by the lateral edge of pectoralis major, the lateral edge of latissimus dorsi and the lower border of the 5th intercostal space
What is the difference between syncope and seizures?
