A&E Flashcards
Acute coronary syndrome (ACS)
Thrombus (platelets) from atherosclerotic plaque blocking a coronary artery.
Unstable angina > NSTEMI > STEMI
ACS: presentation
> 15 mins
- Central crushing chest pain +
- N+V
- Sweaty + clammy
- Feeling of impending doom
- SOB
- Palpitations
Silent MI = no chest pain, diabetic
ACS: investigation
ECG and troponin
- Unstable angina = ACS symptoms, normal tropinin, normal ECG or ECG changes (NSTEMI)
- STEMI = ST-segment elevation, new left bundle branch block
- NSTEMI = raised tropinin, ST segment depression, T-wave inversion
Other Ix:
- Bloods: FBC, U+E, LFTs, lipids and glucose
- CXR for differentials
- Echo to assess LV damage
STEMI definitive management
- Primary percutaneous coronary intervention if symptoms onset < 12hrs and available within 2hrs
- Thrombolysis (e.g. alteplase)
ACS: initial management
CPAIN
C - call ambulance
P - perform ECG
A - Aspirin 300mg
I - IV morphine
N - nitrates (GTN)
NSTEMI definitive management
BATMAN-O
B – Base the decision about angiography and PCI on the GRACE score
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M – Morphine titrated to control pain
A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N – Nitrate (GTN)
O2 if sats <95% without COPD
Secondary prevention for ACS
6As
- Aspirin 75mg once daily
- Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
- Atorvastatin 80mg once daily
- ACE inhibitors (e.g. ramipril)
- Atenolol (or other beta blocker)
- Aldosterone antagonist for those with clinical heart failure
Acute kidney injury (AKI)
Rapid deterioration in kidney function.
NICE 2019 criteria:
- Increase in creatinine > 25micromol/L in 48 hours
- Increase in creatinine > 50% in 7 days
- UO < 0.5ml/kg/hr in at least 6 hours
AKI risk factors
- > 65
- Sepsis
- Chronic kidney disease
- Heart failure
- Liver disease
- Meds (DAMN-G Diuretics, ACEi/ARB, Metformin, NSAIDs, Getamicin)
Causes of AKIwwwww
Pre-renal, renal, post-renal
- Pre-renal - hypoperfusion e.g. dehydration, shock (e.g. sepsis)
- Renal- kidney disease e.g. glomerulonephritis, acute interstitial nephritis
- Post-renal - obstruction to outflow e.g. kidney stones, BPH, tumours
AKI: investigations
Urinalysis
- Leucocytes + nitrite = infection
- Protein + blood = acute nephritis/infection
- Glucose = diabetes
USS of the urinary tract if post-renal cause suspected.
AKI: Management
- Stop/adjust nephrotoxic drugs
- Adequate fluids (IV or oral)
- IV fluids (dehydration or hypovolaemia)
- Relieve obstruction (e.g. catheter in BPH)
- Dialysis if severe
- Renal specialist if severe or unknown cause
If untreated: fluid overload, heart failure, hyperkalaemia, metabolic acidosis, uraemia > encephalopathy
Anaphylaxis
A medical emergency caused by a type 1 IgE mediated hypersensitivity reaction to an allergen.
Urticaria, angioedema, wheeze, SOB, larynx swelling (stidor), tachy
Anaphylaxis: management
- ABCDE
- IM adrenalin, repeat after 5 min if needed
- Antihistamines, e.g. oral chlorphenamine or cetirizine
Steroids, IV hydrocortisone - Observation, measure mast cell tryptase within 6hrs - risk of biphasic reaction
Abdominal aortic aneurysm
Dilatation of the abdominal aorta > 3cm.
Rupture = bleeding into abdominal cavity
Clinical features:
- Severe abdominal pain that might radiate to back or groin
- Haemodynamic instability
- Pulsatile and expansive abdominal mass
Management for ruptured abdominal aortic aneurysm
- Experienced seniors, vascular surgeons, anaesthetists and theatre teams.
- Haem unstable = straight to surgery, permissive hypotension
- Haem stable - CT angiogram
- Co-morbiditues with poor outcome = discussion with family about palliative care
Arrhythmia (covered in detail in cardiology)
Abnormal heart rhythms
- Cardiac arrest rhythms
- Narrow complex tachycardia
- Broad complex tachycardia
- Atrial flutter
- Prolonged QT interval
- Ventricular ectopics
- Heart block
- Bradycardia
Cardiac arrest rhythms
- Shockable rhythms: ventricular tachycardia, ventricular fibrillation
- Non-shockable: pulseless electrical activity (no pulse but heart rhythm present), asystole
Risk factors for cardiac arrest
-Coronary artery disease
- LV dysfunction (e.g. IHD)
- Age
- Hypertrophic cardiomyopathy
- Meds that prolong QT interval
Management of cardiac arrest
- ABCDE, CPR, call for help, gain IV or IO access
- Shockable: defibrillation (120 to 360 joules) for 2 mins
- CPR (30 compression, 2 breaths for 5 cycles - 2mins)
- After 3 shocks > 300mg amiodarone and 1mg adrenaline
- Repeat adrenalin every 3 - 5 mins
Mangement of non-shockable rhythms
- ABCDE, call 999, gain IV or IO access
- CPR
- Adrenaline 1mg IV or IO
- Repeat dose of adrenalin every 3 to 5 mins
- Defibrillation and amiodrone if change to shockable rhythm
Acute left ventricular failure (actue HF)
- Acute event leading to LV failure to pump blood effectively into systemic circulation.
- Often result of decomplensated chronic HF
Tom tip: acute HF and pulmonary oedema common in acute hospital, pt with SOB and desats, how much fluid given? Able to cope? Dose of IV furosemide to clear excess fluid and resolve sypmtoms
Triggrs of acute LVF/HF
- Iatrogenic (e.g., aggressive IV fluids in a frail elderly patient with impaired left ventricular function)
- Myocardial infarction
- Arrhythmias
- Sepsis
- Hypertensive emergency (acute, severe increase in blood pressure)
Clinical features of acute LVF/HF
- Acute SOB
- Looking/feeling unwell
- COugh with pink/white sputum
- Type 1 resp failure (low O2, low/normal Co2)
Signs: tachycardia, tachypnoea, reduced O2 sats, 3rd heart sound, bilateral basal crackles, hypotension (cardiogenic shock)
Ix acute LVF/HF
- Clinical assessment (Hx, examination and ABCDE if needed)
- ECG (ischaemia and arrhythmias)
- Bloods (anaemia, infection and kidney function), B-type natriuretic peptide, tropnin if MI
- ABG
- CXR (cardiomegaly)
- Echo (assess ejection fraction)
BNP = hormone released from ventricles to relax smooth muscle in blood vessels when the myocardium is overstretched. High levels = heart is overloaded.
Senesitive not specific. -ve = exclude HF, but can be raised in sepsis, PE renal impairment etc.
Management of acute LVF/HF
- Hospital admission
- HDU/ICU if pulmonary oedema or cardiogenic shock
- SODIUM mnemonic
-S - sit up (oxygenate lungs, stop fluid spread) - O - oxygen (for < 95%, maintain 88 - 92% in COPD)
- Diuretics (increases UO)
- I - IV fluids stopped
- U - Underlying cause = treat
- M -monitor fluid balance
Meds: positive inotropes increases contractility for low CO, increases CO and mean arterial pressure (MAP), e.g. after MI
Vasoperssors = vasoconstriction = increase systemic vascular resistance + MAP = better BP and tissue perfusion
Compartment syndrome
Abnormally elevated pressure witihn a fascial compartment, blood flow is cut off to the compartment.
Fascial compartments = muscles, nerves and blood vessels surrounded by fascia (strong, fibrous connective tissue containing the comparmtent contents).
Orthopaedic emergency, needs fasiotomy to relieve pressure and restore blood flow. Otherwise tissue neccrosis.
Clinical features of complartment syndrome
Often due to acute injury e.g. bone fractures, crush injuries), bleeding or oedema increases pressure within the compartment.
Most often legs, but can affect forearm, feet, thighs and butt.
5Ps:
- Pain disproportionate to underlying injury, worsened by passive stretching
- Paraesthesia
- Pale
- Pressure (high)
- Paralysis (late and worrying)
Management of compartment syndrome
- Clinical diagnosis
- Escalate to senior, remove dressing, elevate leg to heart level, good BP (no hypo)
- Needle manometry - measure compartment pressure
- Emergency fasciotomy - cut through fascia in compartment to relieve pressure + debride necrotic tissue
Chronic compartment syndrome
Associated with exertion, pressure in compartment rises with exertion and falls with rest.
Pain, numbness and paraesthesia
Needle manometry before, during and after to confirm diagnosis + fasciotomy
Clinical features of acute exerbation of COPD
Rapidly worsening symptoms
- Cough
- SOB
- Sputum
- Wheezing
- Triggers: viral or bacterial infection
Ix in COPD excerbation
ABG: Respiratory acidosis
- Low pH
- Low pO2 (respiratory failure)
- Raised pCO2
- Rised bicarbonate (chronic retention of CO2)
Other Ix:
CXR (pneumonia), ECG, FBC (infection), U+E, sputum and blood culture (if suspected sepsis(
Management of acute COPD excerbation
1st line
- Regular inhalers or nebulisers (e.g. salbutamol and ipratropium)
- Steroids (e.g. prednisolone)
- Abx if infection
Severe:
- IV amonphylline
- Non-invasive ventilation (NIV)
- Intubation and ventilation with ICU
IV fluids: indications
- Resuscitation (e.g., sepsis or hypotension)
- Replacement (e.g., vomiting and diarrhoea)
- Maintenance (e.g., nil by mouth due to bowel obstruction)
Main types of IV fluids:
- Crystalloids (water + salts or glucose) e.g. 0.9% NaCl, Hartmann’s solution
- Colloids = larger molecules remaining in intravascular space longer e.g. human albumin solution - unlikely to prescribe
Resuscitation IV fluids
- Hypovolaemic patient
- Isotonic fluids e.g. 0.9%, Hartmann’s solution, Plasma-Lyte 148
- ABCBE to determine fluid status (e.g. hypotension, tachy, >2s cap refill)
- Tx: initial 500ml fluid bolus over 15 mins (STAT) then ABCDE, repeat 250 - 500ml bolus if needed then reasses, then seek expert help if no improvement, particularly if >2L fluids
Remember! No rapid bolus with K+, as K+ infusion can’t exceed 10mmol/L
Maintenance IV fluids
- If pt cannot tolerate oral fluids e.g. NBM or bowel obstruction
NICE recommendations approx.:
- 25 – 30 ml / kg / day of water
- 1 mmol / kg / day of sodium, potassium and chloride
- 50 – 100 g / day of glucose (this is to prevent ketosis, not to meet their nutritional needs)
Daily monitoring to ensure correct Na, K, Ca2+, Mg, haemoglobin, haematocrit, clotting factors, platelets etc.
Based on ideal weight, NOT actual BMI
Caution in elderly/frail pts, hyper/hyponatraemia, HF, renal/liver impairment
Epistaxis (nosebleeds)
Most often originates from Kiesselbach’s plexus in Little’s area. Nasal mucosa at front of nose and very vascular.
Common exam question is where is the most likely location of the bleeding?
Triggers of epitaxis (from benign to serious)
- Nose picking
- Colds
- Sinusitis
- Vigorous nose-blowing
- Trauma
- Changes in the weather
- Coagulation disorders (e.g., thrombocytopenia or Von Willebrand disease)
- Anticoagulant medication (e.g., aspirin, DOACs or warfarin)
- Snorting cocaine
- Tumours (e.g., squamous cell carcinoma)
Presentation and management of epitaxis
Usually unilateral, bilateral might indicate posterior bleeding = increased risk of aspiration
If blood swallowed = vomit blood
Management of epitaxis
Usually self-resolving.
Recurrent = Ix for thrombocytopenia/clotting disorder
If bleeding > 10 - 15 mins/severe/bilateral/haem unstable = hospital for
- nasal pack with nasal tampons/inflatable packs
- Nasal cautery with silver nitrate sticks
- Prescribe naseptin nasal cream to reduce inflammation
How to advise patients on maangement of nosebleed in exam
- Sit up and tilt the head forwards (tilting the head backwards is not advised as blood will flow towards the airway)
- Squeeze the soft part of the nostrils together for 10 – 15 minutes
- Spit out any blood in the mouth, rather than swallowing
GI perforation
A defect in the wall of the bowel, stomach or oesophagus that allows the contents to leak out.
Causes of GI perforation
Upper GI tract:
- Oesophageal or gastric malignancies
- Peptic ulcer disease
Iatrogenic e.g. surgery/endoscopy
Lower GI tract:
- Colorectal cancer
- Bowel obstruction
- Colitis (e.g. inflammatory bowel disease)
- Appendicitis
- Iatrogenic e.g. colonoscopy
- Mesenteric ischaemia
- Metastatic disease
Clinical features of GI perforation
- Severe sudden abdominal pain, Nausea + vomiting
- Signs: peritonism+, shock (hypotension+tachycardia), tachypnoea, fever
+Guarding, rebound tenderness, rigidity on abdo palpation
Investigations for GI perforation
- Blood gas - lactate + pH
- ## Pregnancy test
- Bloods: FBC, CRP, clotting screen and G+S in case of surgery, blood cultures if infection suspected
- CT with contrast to identify and locate perforation
Management of GI perforation
Conservative: NBM, urgent surgical review, ICU if organ failure due to sepsis
- ## Medical: IV broad-spectrum abx, fluid resus, analgesia and antiemetic (maybe parenteral)
- Surgical - most cases need laparotomy (washout, identify cause and repair)
Hypothermia
Core (rectal) temp <35
- Mild: 32.2 - <35 (+/- shivering)
- Moderate: 28 - 32.1
- Severe: < 28 (no shivering)
Ensure low threashold of suspicion and low-reading thermoeter
Causes of hypothermia
Combination of factors:
- Impaired homeostasis e.g. age-related reduction in thermoregulation
- Pathology affecting thermoregulation e.g. pneumonia, MI, HF
- Autonomic neuropathy e.g. diabetic
- Low room temp e.g. poverty, homeless
Presentation of hypothermia
Symtoms: confusion, agitation, reduced GCS, coma
Signs: brady, hypotension, arrhythmias (AF, VT, VF)
Hx: fall with long-lie, homeless, alcohol/drugs use
Rewarm + re-exam, many people have returned to life when warm despite no vital signs.
Management of hypothermia
- ABCDE, ensure safe airway
- Warm, humidifed O2
- Ventilation if reduced GCS, reduced pO2 and increased pCO2
- Slow rewarming = blankets or hot air duvet, aim core temp increase of 0.5C/h
- Monitor HR, BP, RR. Increase HR, decrease BP = shock
- Rapid rewarming if CV instability/arrest, warm fluid lavage + intravascular warming
- Monitoring for arrhythmia
Rewarming too quickly = peripheral vasodilation + shock
Allergic disorder (also applies to GP and respiratory)
Range of conditions featuring hypersensitivity of the immune system to allergens.
Aka atopy - predisposition to atopic conditions e.g. allergic rhinitis, eczema, asthma and food allergies
Often type-1 hypersensitivity reactions - IgE mediated.
Clinical features of allergic reaction
- Urticaria
- Angioedema (eyes, lips, mouth, throat)
- SOB + wheeze
- Itchy skin/eyes
- Sneezing
- Rhinorrhoea
- Worsening asthma/eczema
Important aspects of history for allergy
Detailed hx is most accurate way to establish dx!
- Timing afrer exposure to allergen
- Previous + subsquent exposure and reaction to allergen
- Symptoms of rash, swelling, breathing difficulty, wheeze and cough
- Previous personal and family history of atopic conditions and allergies
Used zero to finals paediatric allergy page as could not find any other source.
Investigations for allergy (a good history is the most important1)
- Skin prick test
- RAST test - blood tests for total and specific IgE
Both test for sensitation NOT allergy! Unreliable and misleading. - Patch testing in allergic contact dermatitis
- Gold standard is food challenge testing! Limited availibility and resource intensive
Management of allergy
- Avoid triggers
- Regular hoovering, sheet + pillows change in house mite allergy
- Prophylactic antihistamines useful in unavoidable contact e.g. hayfever
- Adrenalin auto-injector for pts at risk of anaphylaxis
- Immunotherapy at specialist centres, where patients are gradually exposed to increasing allergen levels to build tolerance
Post-exposure:
- Antihistamines (e.g. cetirizine)
- Steroids (e.g. oral prednisolone)
- IM adrenalin
- Monitor for progrression to anaphylaxis
Necrotising fasciitis
- Rapidly progressive infection of the deep fascia > subcutaneous tissue necrosis.
- Mainly group A B-haemolytic strep, but often polymicrobial
- Systemically very unwell (very high inflamm, markers + lactate) despite resus, disportionate to wound apperance, intense pain in affected area + muscles
Mx: urgent radical debridement +/-amputation in theatre and IV abx (e.g. benylpenicillin and clindamycin (check local guidelines).
Non-accidental injury (NAI)
Physical harm inflicted on a child or as a result of the caregiver to protect them from this harm.
Risk factors include:
- DV, previous child maltreatment
- Caregiver substance/alcohol misuse
- Poverty
- Children in care system
- Children and young people with disabilities
Presentation of NAI
- Inconsistencies in caregiver narrative e.g. changing stories, severity/type of injury not matching with story
- Delayed presentation
- Unwitnessed injury
Examination: - Injuries of varying ages
- Burns, scalds, bruises
- Retinal/subconjunctival haemorrhage
- FGM
- Torn frenum - head injury/force feeding
Investigations for NAI
- Detailed history + body map
- Comprehensive radiological skeletal survey to identify rib/clavicle/finger fractures, metaphyseal corner fractures (twisting limb)
- Bloods for dffierentials e.g. clotting disorders or haematological malignancies
Mangement of NAI
- Report to senior and safeguarding lead
- Measures: admit child for safeguarding while Ix continue
- Clear documentation
- Social care liaison
Female Genital Mutilation
Intentional injuries, cuts or alterations to female genitals without medical indication.
Illegal in the UK
Contact 999 if you suspect a patient is at immediate risk of FGM, or calll 101 (police or NSPCC if not immediate
Pancytopenia
Reduction in all major cell lines: red, white, platelets.
Causes:
1) Reduced marrow production: aplastic anaemia, infiltration in leukaemia/lymphoma, megablastic anaemia
2) Increased peripheral destruction in hypersplenism
Pacytopenia: define agranulocytosis
Absence of granulocyte (neutrophils, basophils or eosinophils) production > risk of fatal infection
Causes: clozapine, carbimazole etc.
Pts often present with fever or sore throat (wcc ≤ 0.5 x 10^9L) = NEUTROPENIC SEPSIS - A MEDICAL EMERGENCY!
Stop drug, start neutropenic sepsis regimen (including sepsis 6) and consider granulocyte colony stimulating factor G-CSF)
From Oxford Handbook of Clinical Medicine
What is invovled in the sepsis 6 pathway?
Three tests:
- Serum lactate
- Blood cultures
- Urine output
Three treatments:
- Oxygen therapy (94-98%) or 88-92% in COPD)
- Empirical broad-spectrum antibiotics
- IV fluids
Neutropenic sepsis
- Sepsis in someone with neutrophil count < 0.5x10^9/L
- Temp > 38 in pt undergoing cancer or immunosuppressant tx is this until proven otherwise
- Causes: chemo, methtrexate (RA), sulfasalazine (RA), infliximab etc.
- Tx: follow local neutropenic sepsis policy, broad spectrum abx e.g. piperacillin with tazobactam (tazocin), other tx same as sepsis but closer monitoring and lower threshold for escalation
From zero to finals
Sepsis
When the body launches a large immune response to an infection > systemic inflammation + organ dysfunction
Pathophysiology of sepsis
Macrophages, lymphocytes and mast cells identify pathogens and release cytokines = immune activation:
- Vessel endothelial lining = leaky = oedema of extracelluar spaces > hpoperfusion of organs
- Activation of coagulation pathways, fibrin deposits and blood clots throughout circulation = hypoperfusion and DIC+
- Tissue undergo anaerobic respiration > increased lactate and metabolic acidosis
+Blood clots in vessels > DIC = thrombocytopenia and haemorrhage
Risk factors for sepsis
- Very young/old (<1 or >75)
- Chronic conditions e.g. COPD, diabetes
- Chemo, immunosuppressants, steroids
- Surgert, trauma or burns
- Pregnancy and childbirth
- Cathethers and central lines
Presentation of sepsis
NEWS2 score to identify acutely unwell patients: temp, HR, RR, O2, BP and consciouness
- Possible source of infection
- Reuced urine output
- Mottled skin
- Cyanosis
- Arrhythmia e.g. new AF
- Non-blanching rash (meningococcal septicaemia
- Tachypnoea = early sepsis sign
- Elderly pts usually non-specific e.g. confusion, drowsiness
Neutropenic/immunosuppressed pts can have normal obs but be life-threateningly unwell
Investigations for suspected sepsis
- FBC for WCC and neutrophils
- U+Es for AKI
- LFTs for liver infection
- CRP
- Blood glucose
- Clotting for DIC
- Blood cultures for bacteraemia
- ABG for lactate, pH and glucose
For source of infection: urine dipstick and culture, CXR, CT if intra-abdo infection suspected, LP for meningitis/encephalitis
Mangement for sepsis
- Each hospital has sepsis protocol and pathway
- Escalate to senior
- HDU/ICU if needed
NICE stratifies into low, med and high risk patients
- High risk - urgent attention and mx
- Moderate risk = mx in community if safe + safety-netting
Suspected sepsis = assessment and tx within 1 hour, sepsis six (see card)!
Testicular torsion
Twisting of spermatic cord with rotation of the testicle
Urological emergency! Delay = ischaemia, necrosis, infertility
Presentation of testicular torsion
- Typically teenage boy after playing sports
- Unilateral testicular pain
- Abdominal pain (sometimes only symptom)
- Vomiting
Examination: firm swollen, retracted testicle, absent cremasteric reflex, abnormal testicular lie (horizontal - Bell-Clapper deformity)
Management of testicular torsion
- NBM
- Analgesia
- Urgent senior urology assessment
- Surgical exploratiob of scotum
- Orchiopexy (correcting testicle position and fixation)
- Orchidectomy if surgery delayed or necrosis
Scrotal USS to confirm dx, but don’t delay tx!
Toxic Shock Syndrome
Cause: group A strep or staph aureus, endotoxin-mediated
Menstrual: prolonged tampon use
Non-menstrual: postpartum vaginal/C-section wound infection
Clinical features: severe pain in extremity, fever, localised swelling/erythema, hypotension
RFs: diabetes, alcohol dependency, minor trauma/surgery, prolonged tampon use
Ix: 1st line is microscopy and blood, wound, fluid, tissue culture
Tx:
- Fluid resus, ICU
- Strep: clindamycin + benzylpenicillin/vancomycin
- S.aureus: clindamycin +oxacillin/nafcillin/vancomycin
