Emergency Medicine Flashcards
AAA History?
Severe abdominal and back pain, collapse/feeling faint.
Previous heart disease/↑BP, aged >50 years, male.
AAA Examination?
Expansile mass, unwell, ↓BP, ↑HR, ↑RR, ↓leg pulses, pale, sweating, cool extremities, distension, tenderness.
AAA Investigations?
None if unstable. Urgent USS/urgent CT.
Management of AAA?
Fast bleep for senior help and vascular surgeon immediately. Order urgent O -ve blood and urgent X-match 8 units.
O2 15 L/min; resuscitate – large bore IV access for bloods and STAT colloid/blood (keep systolic BP 90-100mmHg).
Prepare to transfer to theatre or interventional radiology suite
Observations every 15 min
Those unfit for intervention require palliative care.
Appendicitis history?
Central, abdominal colicky pain worsening over 1-2 days then developing into constant RIF pain. Worse on moving.
Anorexia, nausea, vomiting, may have constipation, diarrhoea, dysuria, oliguria
Appendicitis examination?
Slight temp, ↑HR +/- ↓BP
RIF tenderness +/- guarding/rebound/rigidity. RIF pain on palpating LIF (Rovsing’s sign)
PR tender on right
Appendicitis investigations?
Useful triad = ↑WCC, neutrophils >75%, ↑CRP.
Blood cultures (if pyrexial)
US and contrast-enhanced CT – reduce laparotomy rates, but must be balanced against risk of radiation and local resources.
Group and save - surgery.
Management of appendicitis?
Surgery – NBM, IV fluids, analgesia, IV abx (co-amoxiclav 1.2g/8h IV).
If peritonitic, send for immediate surgery. Otherwise reassess regularly whilst awaiting surgery.
If diagnostic uncertainty a short period of safe observation +/- imaging can be informative.
Bowel obstruction history?
Vomiting (may be faeculant), colicky abdo pain, pain may improve with vomiting.
Constipation (may be absolute – no flatus or stool), bloating, anorexia, recent surgery.
Bowel obstruction examination?
↑HR, ↓BP, ↑RR, distended abdomen, absent or tinkling bowel sounds, peritonitis, scars from previous surgery, hernias.
Causes of bowel obstruction? (outside bowel)
Adhesions, hernias, masses, volvulus
Causes of bowel obstruction? (within bowel wall)
Tumours, IBD, diverticular disease, infarction, congenital atresia, Hirschprung’s disease
Causes of bowel obstruction? (inside bowel lumen)
Impacted faeces, FB, intussusception, strictures, polyps, gallstones
Causes of bowel obstruction? (paralytic ileus - pseudo-obstruction)
Post-op, electrolyte imbalance, uraemia, DM, anticholinergic drugs
Bowel obstruction investigations?
Bloods - ↑WCC and ↑amylase +/- acidosis.
AXR – look for distended bowel (?small or large) or volvulus
Erect CXR - ?free air
General management of bowel obstruction?
May need fluid resuscitation and analgesia; treat according to type and location of obstruction.
Management of bowel obstruction? - Strangulated (constant severe pain + peritonitis)
Requires urgent surgery especially if caused by a hernia.
Management of bowel obstruction? small bowel (early vomiting, late constipation)
Conservative – NBM, NG tube, IV fluids until obstruction resolves. Surgery if deteriorates.
Management of bowel obstruction? Large Bowel (early constipation, late vomiting)
IV fluids, NBM and refer to senior surgeon.
Management of bowel obstruction? Paralytic Ileus
Lack of pain
USS/contrast enema/CT to exclude mechanical obstruction. NBM, NG tube, IV fluids. Correct electrolyte abnormalities.
Diverticulitis history?
Abdominal pain/cramps (usually left sided, improves with bowel opening), irregular bowel habit, flatus, bloating, PR bleeding.
Diverticulitis examination?
↑temp, ↑HR, ↓BP, LIF tenderness, +/- peritonitis, distension.
Diverticulitis examination?
↑WCC, ↑CRP
CT/colonoscopy for indirect/direct visualisation
Diverticulitis management?
NBM, analgesia, IV fluids and abx (co-amoxiclav 1.2g/8h IV)
Ectopic pregnancy - when should you consider?
CONSIDER IN EVERY WOMAN OF CHILD-BEARING AGE PRESENTING WITH COLLAPSE, ACUTE ABDO PAIN +/- PV BLEEDING
Ectopic pregnancy history?
Usually presents at 6-9wk gestation.
Abdominal pain, shoulder tip/back pain, PV bleeding, recent amenorrhoea, dizziness.
Ruptured ectopic = collapse, shock, peritonism.
Ectopic pregnancy examination?
Abdo: unilateral iliac fossa pain +/- mass; if rupture, guarding. ↑HR, ↓BP.
PV: bleeding, extreme cervical pain.
Risk factors for ectopic pregnancy?
↑maternal age, previous ectopic, tubal surgery, previous STIs/PID, IUCD, assisted conception techniques, smoking.
Differentials for ectopic pregnancy?
Miscarriage, appendicitis, pelvic infection, ovarian cyst.
Investigations ectopic pregnancy?
Bloods - Β-hCG (serum and urine), FBC
USS – foetal sac/pole in the adnexae, free fluid.
Relevant to Initial Management - Group and save/X-match
Management of ectopic pregnancy?
Emergency - IV access (14-16G), IV fluids and urgent referral to gynae.
Medical - Methotrexate used for small ectopics in stable patients.
Surgical - Laparoscopic/open salpingectomy/salpingostomy/oophorectomy.
Miscarriage history?
Vaginal bleeding, crampy lower abdominal pain, nausea, vomiting, dizziness.
Miscarriage examination?
May be shocked; abdominal tenderness suggests ectopic.
PV - Check size of uterus, exclude adnexal tenderness; speculum -open/closed cervical os, clots, products of conception.
Causes of micarriage?
Threatened, inevitable, missed, incomplete, complete
Investigations for miscarriage?
Bloods – FBC, group and save, β-Hcg
Urine - β-Hcg
USS - transvaginal
Exclusion - If marked abdo/cervical tenderness – exclude ectopic by USS and serial serum β-Hcg.
Management of miscarriage?
If Shocked - Insert grey cannula, fluid resuscitate and remove products of conception from os (can cause vasovagal); ergometrine 0.5mg IM given for severe bleeding. Offer all patients analgesia.
Ovarian cyst history?
Severe, sudden onset lower abdominal pain, iliac fossa pain radiating to right flank, nausea, vomiting, fever.
Ovarian cyst examination?
Abdo – tenderness
PV – adnexal tenderness
Risk factors for ovarian cyst?
Developmental abnormalities, early pregnancy, women undergoing hormonal stimulation for IVF.
Differentials for ovarian cyst?
Appendicitis, diverticulitis, ectopic pregnancy, UTI
Investigations ovarian cyst?
Urine – dipstick +/- MSU
USS
Exclusion - Urine and serum β-Hcg (to exclude pregnancy/ectopic)
Management of ovarian cyst?
IV access for fluids, analgesia; laparoscopy if not settling.
Complications of ovarian cyst?
Infection, peritonitis, adhesions, infertility (rare)
Acute pancreatitis history?
Constant severe epigastric pain radiating to back, improved by sitting forward, nausea, vomiting, anorexia.
Acute pancreatitis examination?
↑HR, ↓BP, ↑temp, cold extremities, epigastric tenderness with peritonitis, abdominal distension, ↓bowel sounds, mild jaundice.
Cullen’s sign (bruised umbilicus), Grey-Turner’s sign (bruised flanks).
Causes of acute pancreatitis?
I GET SMASHED
Idiopathic, gallstones (50%), ethanol (25%), trauma, steroids, mumps, autoimmune, scorpion bites (rare), hyperlipidaemia, hypercalcaemia, hypothermia, ERCP, drugs (thiazide diuretics)
acute pancreatitis investigations?
Bloods - ↓Hb, ↑WCC, ↑↑↑lipase (or amylase), ↑glucose, ↓Ca2+, deranged clotting (+/- DIC), LFT
USS - ?gallstones
CT – if diagnosis in doubt
Management of acute pancreatitis?
Emergency - IV fluid resuscitation, O2, analgesia, urinary catheter, NBM, NG tube.
Escalation - If severe involve ICU and plan ERCP if gallstone aetiology.
Routine - Monitor fluid balance, obs, glucose. Daily U+E, FBC, CRP, prophylactic LMWH.
PID history?
Lower abdominal pain, vaginal discharge, intermesnstrual/postcoital bleeding, pyrexia, dysuria, dysparenuria, nausea, vomiting, infertility, general malaise.
PID examination?
Abdo – tenderness
PV – adnexal tenderness, cervical excitation
PID causes?
Infection and inflammation of upper gential tract commonly with STIs (Chlamydia Grachomatis or Neisseria Gonnorrhoeae)
PID risk factors?
Young age at first intercourse, multiple sexual partners, no barrier contraception, smoking.
PID differentials?
Appendicitis, endometriosis, ovarian cysts, ectopic pregnancy, other STIs, HIV, UTI
PID investigations?
MSU – genital swabs (high vaginal, endocervical, chlamydia) for M, C + S
Bloods – FBC, CRP, cultures
Exclusion - USS – to exclude ovarian cyst
Management of PID?
IV access for fluids + analgesia
Remove IUCD
Antibiotics (ceftriaxone 250mg IM stat, then metronidazole 400mg/12h PO and doxycycline 100mg/12h PO for 14 days)
Refer to GUM clinic for contact tracing
Complications of PID?
Untreated may lead to chronic pelvic pain and infertility; tubo-ovarian abscess, septicaemia, secondary infertility, ectopic pregnancy.
Peptic ulcer disease history?
Burning retrosternal or epigastric pain, worse on bending and lying. Waterbrash, acid reflux, nausea, vomiting, nocturnal cough. Symptoms improved by antacids.
Peptic ulcer disease examination?
Epigastric tenderness (no peritonitis), rarely epigastric mass.
Risk factors for peptic ulcer disease?
Smoking, alcohol, obesity, pregnancy, hiatus hernia, medications (bisphosphonates, calcium antagonists, nitrates, corticosteroids, NSAIDs).
Investigations for peptic ulcer disease?
Urgent endoscopy if ‘red flag’ symptoms (chronic GI bleeding/iron deficiency anaemia, unintentional weight loss, progressive dysphagia, persistent vomiting, epigastric mass) or >55 and persistent/unexplained dyspepsia.
Management of peptic ulcer disease?
1-2 months full dose PPI. 95% duodenal and 80% gastric ulcers are related to H.pylori so ensure eradication.
Repeat endoscopy at 6 weeks to ensure healing – ulcers associated with malignancy.
H. Pylori Eradication
C-urea breath testing – wash-out period of 2 weeks off PPI required.
Treatment
Triple therapy for 1 week – lansoprazole 30mg/12h PO, amoxicillin 1g/12h PO, clarithromycin 500mg/12h PO.
Renal colic history?
Acute onset severe unilateral colicky pain radiating from loin to groin, nausea and vomiting, sweating, haematuria, dysuria, strangury (frequent, painful passage of small volumes of urine with sensation of incomplete emptying); iliac fossa or suprapubic pain suggests another pathology.
Renal colic examination?
↑HR, sweating, patient restless and in severe pain, usually no tenderness on palpation unless superimposed infection.
Causes of renal colic?
Renal stones – always consider other causes of abdo pain, including AAA, especially if no history of renal stones.
Renal colic investigations?
Urine – Hb on dipstick, nitrates suggest UTI β-HCG - if female Bloods – FBC, U+E, Ca2+ KUB – detects 60% stones CT – detects >99% stones
Management of renal colic?
Analgesia (NSAID first, then opioids); if <5mm should pass spontaneously.
If evidence of infection give IV abx (check local policy)
If evidence of infection or hydronephrosis refer urgently to urologist for nephrostomy or stent
UTI history?
Cystitis – frequency, dysuria, urgency, pyuria, haematuria, suprapubic pain.
Pyelonephritis – fever, rigors, vomiting, loin pain
pyelo examination?
Warm peripheries, vasodilation, tachycardia, suprapubic/loin pain.
worrying signs in UTI?
↓BP/shock, temp >40, new renal impairment, elderly patients can be afebrile or hypothermic but heavily bacteraemic.
Risk factors for UTI/pyelo?
Sexual intercourse, catheterisation, DM, immunosuppression, pregnancy, structural abnormalities of urinary tract, stones, elderly.
Investigations for UTI/pyelo?
Urine dipstick – nitrities, leucocytes, blood and protein. MSU culture = gold standard. C+S if clinical suspicion of UTI and in all pyrexial/vomiting children.
Bloods – FBC (↑WCC, ↑Nø), U+E (↑urea + creatinine if outflow obstruction), ↑inflammatory markers, ↑glucose (?DM)
Blood cultures – if ↑temp or systemically unwell
Management of cystitis?
If ↓BP treat as septic shock; otherwise paracetmol (for fever) and consider empirical abx therapy (trimethoprim 200mg/12h PO, or co-amoxiclav 1.2g/8h IV if septic) whilst awaiting sensitivities.
↑oral fluid intake.
Treat for 3 days in simple infection in females, 7 days if structural abnormality, immunosuppressed or male.
Management of pyelo?
↓BP –> treat as septic shock; admit for IV abx if septic, pregnant, frail elderly, immunosuppressed or structurally abnormal urinary tract. Give paracetamol and start empirical abx therapy (eg. Co-amoxiclav 625mg/8h PO or 1.2g/8h IV) whilst awaiting sensitivities.
Increase oral fluid intake.
Treat for 7-10 days.
Acutely ischaemic leg history?
Unilateral painful, tingling, weak limb, worse on raising limb.
Acutely ischaemic leg examination?
Absent pulses, slow cap refill (compare with opposite limb), cold and pale (can be red limb if below heart), reduced power and sensation.
Acutely ischaemic leg causes?
Emboli, thrombosis, dissecting aneurysm, trauma
Acutely ischaemic leg risk factors?
Arterial graft, PVD, previous thrombo-embolism, AF, prosthetic heart valves, recent MI, dehydration, malignancy
Acutely ischaemic leg investigations?
Doppler – will show reduced or absent pulse.
Angiography may demonstrate an obstruction.
Management of acutely ischaemic leg?
Urgent surgery – call senior surgeon who will consider embolectomy, intra-arterial thrombolysis, bypass or amputation.
Emergency - 15 L/min O2 + analgesia (morphine); IV access + IV fluids if dehydrated; may require heparinisation pre- or post-op.
Complications of acutely ischaemic leg?
Amputation, gangrene, hyperkalaemia, renal failure, sepsis.
Cellulitis history?
Hot, sometimes tender area of erythema, usually on leg or face; may be spreading; history of trauma to skin (insect bite, cannula site).
May be systemic effects – fever, anorexia, N+V, diarrhoea.
Cellulitis examination?
Blanching warm spreading erythema (outline area with marker to observe response to treatment), +/- mild oedema, break in the skin, serous discharge, lymphadenopathy in draining nodes, ↑temp, ↑HR, ↑RR.
Causes of cellulitis?
Staph Aureus (may be MRSA), group A streptococci
Cellulitis investigations?
Bloods - ↑WCC and neutrophils, ↑CRP/ESR; blood cultures if pyrexial, D-dimer likely to be raised in infection so not useful in differentiating cellulitis from DVT.
Skin swabs – not usually helpful, but check multisite MRSA swab results.
USS – to exclude DVT (depending on Wells’ score) or ruptured Baker’s cyst
Cellulitis management?
If patient is well – oral abx (flucloxacillin 1g/6h PO; if MRSA, 200mg doxycycline STAT then 100mg/24h PO)
If signs of systemic upset or coexisting disease (DM, IHD, PVD) – admit for short course IV abx (flucloxacillin 1g/gh IV; if MRSA, vancomycin 1g/12h IV).
If profoundly unwell – request senior help and consider necrotising fasciitis.
Painful or restricted eye movement, proptosis or visual disturbance –> orbital cellulitis (ophthalmology emergency).
DVT history?
Unilateral swelling and/or pain
DVT examination?
Warm, red, tender, swollen limb (leg >3cm compared to other calf measured 10cm below tibial tuberosity), pitting oedema.
DVT risk factors?
Age >60 yrs, obesity, recent surgery/immobility/long distance travel, oestrogen (pregnancy, HRT, OCP), PMH or FH of PE/DVT, malignancy, thrombophilia, medical comorbidity (CCF, IBD, active inflammation)
Components of Well’s score for DVT?
Active cancer (or last 6 mths) Leg paralysed or in plaster Recent bed rest >3d or major surgery within 12wks Previous documented DVT Visible collateral superficial veins (not varicose) Pitting oedema Tenderness along veins Whole leg swollen >3cm calf swelling
1 point for each – subtract 2 points if there is another diagnosis more likely (e.g. cellulitis).
Well’s DVT score interpretation?
<1 = unlikely (5.5%) – D-dimer, if +ve –> USS; if -ve, unlikely to be DVT.
> 2 = likely (28%) – arrange USS; LMWH if delay in USS >4h
If score >2 but USS -ve, arrange D-dimer – if +ve, repeat USS in 6-8 days.
DVT investigations?
Bloods – FBC, U+E, D-dimer (if indicated).
ECG/ABG – if suspected PE
Management of DVT?
Commence parenteral anticoagulation (enoxaparin 1.5mg/kg/24h SC) if USS +ve or delayed >4 hours.
If confirmed DVT, start oral anticoagulation.
Complications of DVT?
PE, post-thrombotic syndrome (chronic pain and swelling)
Common joints of gout?
Monoarticular in 90% - great toe, MTP, ankle, knee.
Gout history?
Acute onset painful joint, +/- fever, ↓RoM.
Gout examination?
Swollen, hot, tender, red, painful joint.
Chronic = tophi (white/yellow or skin coloured nodules of urate) over Achilles, elbow, knee or ear.
Gout risk factors?
Age, male sex, thiazide diuretics, red meat, alcohol.
Gout investigations?
Exclusion - Exclude septic arthritis
Bloods - ↑WCC/ESR/CRP
Diagnosis - Joint aspiration - -ve birefringent needle-shaped crystals
X-ray = normal
Management of gout?
Acute attack – rest, high fluid intake, reduce thiazides, alcohol and red meat. NSAIDs (diclofenac 50mg/8h PO) or steroids (pred 40mg/24h PO for 3 days then tapered over 3 wks).
Chronic = allopiurinol (not in acute attack)
Common joints for septic arthritis?
Single knee or hip
Common organisms for septic arthritis?
Staphylococci, Strep Pyogenes; Gram -ve bacilli or fungi in elderly or debilitated; TB.
Septic arthritis history?
Acute onset painful joint, swelling, fever
Septic arthritis examination?
Swollen, hot, tender, red, painful joint, often held slightly flexed, ↓RoM
Risk factors for septic arthritis?
Joint disease, prosthetic joint, immunosuppression, age, DM, trauma.
Septic arthritis investigations?
Bloods - ↑WCC, CRP and ESR, +ve blood culture
Joint Aspiration - ↑WCC, organisms on gram stain, +ve culture
X-ray – as baseline
Management of septic arthritis?
Analgesia + urgent orthopaedic referral
High dose IV abx for >6 weeks (co-amoxiclav 1.2g/8h IV) after diagnostic joint aspiration.
May require repeated aspiration/surgical washout.
Complications of septic arthritis?
Joint destruction, secondary arthritis, septicaemia
Asthma history?
Episodic breathlessness, dyspnoea and wheeze, night or morning cough, excess sputum; triggers may include exercise, NSAIDs, β-blockers, allergens, cold.
FH or personal Hx of atopy (hayfever, eczema, asthma).
Asthma examination?
Wheeze, prolonged expiration, tachypnoea, hyperinflated chest
Asthma investigations?
PEFR – reduced in acute setting compared with best or predicted based on age/height.
ABG – normal or ↓PaO2 with a ↓PaCO2 due to hyperventilation – beware normal/rising CO2 –> ?pt tiring
CXR – hyperexpanded, exclude pneumonia and pneumothorax
Severe asthma?
Incomplete sentences, PEFR <50% of best, HR >110, RR >25
Life-threatening asthma?
PEFR <33% of best, silent chest, sats <92%, PaO2 <8kPa, normal PaCO2, poor respiratory effort, exhaustion, cyanosis, altered GCS, arrhythmia
Near-fatal asthma?
CO2 retention – CALL ICU
Management of asthma?
Sit up – give 15L/min O2.
Salbutamol 5mg NEB +/- ipratropium 500mcg NEB and prednisolone 40mg PO (or hydrocortisone 200mg IV) – drive nebuliser mask from O2 supply, not air.
Repeat salbutamol 2.5mg nebs every 10-15 mins + reassess PEFR/sats.
If not improving…
- Senior help
- Consider ICU input
- Aminophylline 5mg/kg IV bolus over 20min
- Mg2+ sulphate 2g (8mmol) IV over 20 mins
Admit if PEFR <75% predicted after 1 hour – gradually reduce O2 and change nebs to inhalers over several days.
COPD exac history?
Breathlessness, cough, ↑sputum, tight chest, confusion, ↓exercise tolerance
COPD exac examination?
Wheeze, cyanosis, barrel-chested, poor expansion, tachypnoea
COPD exac investigations?
ABG – compare with previous samples and pay close attention to FiO2; repeat after 30 mins in seriously ill patients.
CXR – hyperextended, flat diaphragm (look for evidence of infection, pneumothorax or bullae)
COPD exac management?
Sit patient up and given patient minimum amount of O2 to maintain sats >88% (PaO2 8kPa).
Salbutamol 5mg +/- ipratropium 500mcg nebs (drive by air, leave nasal cannula on under mask if necessary) and prednisolone 30mg PO (or hydrocortisone 200mg IV).
Sputum for M, C + S.
Use ABG results to guide further treatment
Normal (for them) – continue current O2 and give regular nebs
Worsening hypoxaemia - ↑FiO2, repeat ABG <30 min, watch for confusion which should prompt a repeat ABG sooner; consider NIV.
↑CO2 retention or ↓GCS – request senior help urgently – consider ICU input, aminophylline 5mg/kg IV bolus over 20 mins, NIV.
Antibiotics
Consider if patient has increase SoB, fevers, worsening cough, purulent sputum, or focal changes on CXR.
Doxycycline 200mg PO loading then 100mg/24h PO or amoxicillin 500mg/8h PO.
Pneumonia history?
Cough, increased sputum (coloured), pleuritic chest pain, breathless, haemoptysis, fever, unwell, confusion, anorexia
Pneumonia examination?
↑temp, ↑RR, ↑HR, ↓sats, unequal air entry, reduced expansion, dull percussion, bronchial breathing
Pneumonia severity?
CURB-65
Confusion Urea >7mmol/L RR >30/min Blood pressure <90 or DBP <60 Age >65 yrs
CURB-65 interpretation?
0-1 = Low severity - Risk of death <3% 2 = Moderate severity – Risk of death 9% 3-5 = High severity – Risk of death 15-40%
Common organisms in CAP?
Step pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae. Staph Aureus, Maroxella catarrhalis, Chlamydia.
Viruses 15%.
Common organisms in HAP?
Gram -ve enterobacteria (pseudomonas, klebsiella, E.coli), S.Pneumoniae, S.Aureus (+ MRSA).
Pneumonia investigations?
Bloods - ↑WCC, neutrophils, CRP
Blood Cultures – if CURB-65 >2
Sputum Cultures – if CURB-65 >3
ABG - ↓PaO2 (↓PaCO2 due to hyperventilation but not if tiring or COPD)
CXR – may show focal consolidation; repeat at 6wks if ongoing symptoms or high risk for malignancy.
Pneumonia management?
Sit up + give O2 as required. Give Abx according to local guidelines.
Look for dehydration and give IV fluids. Most can be switched to PO abx by day 3.
If symptoms not resolving, repeat CRP + CXR to exclude pleural effusion/empyema.
CAP/HAP - Antibiotic therapy according to CURB-65?
CAP, CURB65 = 1
Amoxicillin 500mg-1g/8h PO
CAP, CURB65 = 2
Amoxicillin 1g/8h PO/IV + clarithromycin 500mg/12h PO/IV
CAP, CURB65 >3
Co-amoxiclav 1.2g/8h PO/IV + clarithromycin 500mg/12h PO/IV
HAP
Co-amoxiclav 1.2g/8h IV (if severe, Tazocin 4.5g/8h IV)
Pneumothorax history?
Breathlessness +/- chest pain
Pneumothorax examination?
Hyper-resonant and reduced air entry on affected side, tachypnoea, may have tracheal deviation or fractured ribs.
TENSION PNEUMOTHORAX
Hypotensive, tachycardic, tachypnoeic, unilateral hyperresonance and reduced air entry.
Risk factors for pneumothorax?
Primary (Spontaneous)
Thin, tall, male, Marfan’s, recent central line, pleural aspiration or chest drain
Secondary (In presence of lung disease or injury)
COPD, asthma, infection, trauma, mechanical ventilation
Pneumothorax investigations?
CXR – lung markings not extending to the peripheries, line of pleura seen away from peripheries.
Simple pneumothorax management?
Sit up and give 15 L/min O2.
Primary
If >2cm/breathless – aspirate with 16-18G cannula –> chest drain/discharge.
Secondary
If >2cm/breathless – chest drain + admit
If 1-2cm – aspirate + admit
Everyone else – admit, high flow O2, observe for 24 hours.
Tension pneumothorax management?
Sit up and give 15 L/min O2.
Treat prior to CXR
Insert grey/orange cannula into 2nd intercostal space, midclavicular line. Listen for a hiss and leave it in situ; insert a chest drain on the same side.
If no hiss, leave cannula in situ and consider placing a 2nd cannula or alternative diagnosis.
PE history?
Often no symptoms except breathlessness; may have pleuritic chest pain, haemoptysis, dizziness, leg pain.
PE examination?
↑JVP, ↑RR, ↑HR, ↓BP, RV heave, pleural rub +/- pyrexia. Tachycardia and tachypnoea may be only clinical signs.
Wells’ score for PE?
Signs/symptoms of DVT - 3
PE most likely clinical diagnosis - 3
HR > 100 - 1.5
>3d immobilisation or surgery in past 4 weeks - 1.5
Previous DVT/PE - 1.5
Haemoptysis - 1
Malignancy (current treatment or in past 6 months or palliative) - 1
Wells’ score for PE interpretation?
<4 = low risk – test for D-dimer. If elevated --> CTPA. >4 = high risk. Proceed to CTPA (with LMWH if scan can’t be done immediately
PERC score for PE?
Age <50 years Pulse <100 BPM SaO2 >95% on room air No haemoptysis No exogenous oestrogen use No prior VTE No surgery or trauma requiring hospitalisation in past 4 weeks No unilateral leg swelling
If all criteria negative and pre-test probability <15%,, PE can be ruled out.
PE investigations?
D-dimer – raised in many situations, whilst normal D-dimer must be interpreted in clinical context.
ECG – sinus tachy, RBBB, inverted T waves V1-V4 or S1Q3T3.
ABG - ↓CO2 +/- ↓O2 if large
CT-PA – definitive imaging modality
V/Q scan – may be used e.g. in renal failure
PE management?
Acute
Sit up (unless ↓BP) and give 15 L/min O2. If life threatening seek immediate senior support, arrange urgent CT-PA +/- echo and consider thrombolysis.
Otherwise, parenteral anticoagulation (enoxaparin 1.5 mg/kg/24h SC) and pain relief; IV fluids if hypotensive.
Chronic Oral anticoagulation (warfarin – INR 2-3) for at least 3 months.
Pulmonary oedema history?
Dyspnoea, orthopnoea, PND, frothy sputum, coexistent dependent oedema or previous heart disease.
Pulmonary oedema examination?
↑JVP, tachypnoea, fine inspiratory basal crackles, wheeze, pitting cold hands and feet; oedema (ankles and/or sacrum) suggests right heart failure
Pulmonary oedema investigations?
Bloods – look for anaemia, infection or MI; FBC, U+E, CRP, cardiac markers; BNP (normal levels unlikely in cardiac failure)
ABG – may show hypoxia
ECG – exclude arrhythmias and acute STEMI, may show old infarcts, LV hypertrophy or strain
CXR – cardiomegaly (not if AP projection), signs of pulmonary oedema
Echo – poor LV function/ejection fraction
Management of pulmonary oedema?
Acute
Sit up and give 15 L/min O2. If attack is life threatening call an intensivist early as CPAP and ICU may be required.
Monitor HR, BP, RR and O2 sats whilst giving furosemide 40-120mg IV +/- diamorphine (repeat every 5 minutes up to 5mg max, watch the RR).
If further treatment required, be guided by blood pressure:
Systolic >100 – give 2 sprays of sublingual GTN followed by IV nitrate infusion (e.g. GTN starting at 4mg/h and increasing by 2mg/h every 10 min – aiming to keep systolic >100)
Systolic <100 – patient is in shock, probably cardiogenic. Get senior help as inotropes required. Do not give nitrates.
Wheezing – treat as for COPD alongside above treatment
No improvement – Give furosemide up to 120mg total (more if chronic renal failure) and consider CPAP. Insert urinary catheter to monitor urine output +/- CVP monitoring. Request senior help. Consider HDU/ICU.
STEMI history?
Central, crushing, heavy chest pain (>20 mins) +/- radiating to left arm/jaw, shortness of breath, nausea, sweating, palpitations, anxiety
STEMI examination?
Examination
Tachycardia, cool and sweaty (‘clammy’) +/- LV failure or hypotension
STEMI risk factors?
Smoking, obesity, DM, hypertension, hypercholesterolaemia, FH, previous IHD
STEMI investigations?
ECG – ST elevation (>1mm in 2 or more contiguous limb leads or >2mm in chest leads) or new LBBB; subsequent Q waves +/- T wave inversion
CXR – cardiomegaly, signs of LV failure
Cardiac Markers – will be raised but treatment should not be withheld as ECG findings and history alone are sufficient to make diagnosis
Management of STEMI?
GOAL = PCI within 12 hours of onset of symptoms – seek senior help.
O2 – 15 L/min
Aspirin – 300mg
Clopidogrel – 300mg
Diamorphine – 2.5-5mg IV
Antiemetic
GTN – two puffs SL/5min until pain free; infusion if ongoing pain after 3 SL doses provided not hypotensive
B-blockade – bisoprolol 10mg/PO – limits infarct size and reduces mortality but avoid in COPD, hypotension and overt failure.
Complications of STEMI?
Dysrhythmias (AV block, bradycardia, VF/VT), LVF, valve prolapse, ventricular septal rupture, ventricular aneurysm formation, pericarditis, Dressler’s syndrome, recurrent pain
NSTEMI history/exam/risk factors?
Similar to STEMI; patients usually older, with more co-morbidities.
NSTEMI investigations?
ECG – ST depression, inverted T waves; subsequent evolution of changes +/- T wave inversion
CXR – cardiomegaly, signs of LV failure
Cardiac Markers – differentiate from unstable by elevated troponin – taken on presentation and 12 hours after worst pain.
NSTEMI management?
O2 – 15 L/min Aspirin – 300mg Clopidogrel – 300mg Diamorphine – 2.5-5mg IV Antiemetic GTN – two puffs SL/5min until pain free; infusion if ongoing pain after 3 SL doses provided not hypotensive Anticoagulation – with fondaparinux β-blockade – bisoprolol 10mg/PO – limits infarct size and reduces mortality but avoid in COPD, hypotension and overt failure.
Risk stratification in NSTEMI?
Scoring algorithms – Thrombolysis in Myocardial Infarction (TIMI) risk score, The Global Registry of Acute Coronary Events (GRACE) algorithms.
Risk scores can be calculated on admission (to predict in hospital and 6 month mortality) or on discharge (to predict 6 month mortality).
High-risk – need a CCU, bed, consideration for GP IIb/IIIa inhibitors and urgent catheterisation (within 96hrs)
Low/Intermediate risk – require risk observation to ensure pain free, then further stratification using exercise ECG, coronary calcium scoring or stress imaging to determine need for cathterisation.
Unstable angina history, examination and risk factors?
Overlap with other forms of ACS; typically, episodes of angina occurring on minimal provocation or at rest, with poor response to GTN; more frequent and more severe pain than patient’s ‘usual’ angina; few symptoms or signs between episodes of pain.
Diagnosis is based upon typical history in presence of ECG changes, but without subsequent elevation of cardiac markers.
Investigations in unstale angina?
ECG – ST depression, flat or inverted T waves with dynamic changes over time, signs of previous MI.
Cardiac Markers – not elevated
Management of unstable angina
Same as NSTEMI.
Aortic dissection history?
Sudden onset severe chest pain, anterior or interscapular, tearing in nature, dizziness, breathlessness, sweating, neurological deficits.
Aortic dissection examination?
Unequal radial pulses, tachycardia, hypotension/hypertension, difference in brachial pressures >15 mmHg, aortic regurgitation, pleural effusion (L>R), neurological deficits from carotid artery dissection,
Aortic dissection risk factors?
Smoking, obesity, DM, ↑BP, ↑cholesterol, FH, previous IHD
Aortic dissection investigations?
ECG – may be normal or show LV strain/ischaemia
CXR – classically widened mediastinum >8cm (rarely seen), irregularity of aortic knuckle and small left pleural effusion can develop from blood tracking down.
Echo – May show aortic root leak, aortic valve regurgitation or pericardial effusion. Also consider MRI/CT/conventional angiography.
Management of aortic dissection?
Seek senior help.
If hypotensive, treat as shock – O2 15 L/min, two large bore cannulae, X-match 6 units, analgesia (IV opioids).
If hypertensive, aim to keep systolic BP <100 mmHg – oral therapy with ACEi or CCB.
Further treatment = surgery (type A – ascending aorta) or conservative management (type B – only descending aorta)
Alcohol withdrawal history?
12-36h post-alcohol; anxiety, shaking, sweating, vomiting, tonic-clonic seziures.
3-4d post-alcohol; delirium tremens may develop; coarse tremor, confusion, delusions, hallucinations (untreated mortality 15%)
Alcohol withdrawal examination?
Hypertension, tachycardia, pale, sweaty, tremor, hypoglycaemia, delirium tremens, pyrexia.
Alcohol withdrawal investigations?
Bloods – may have ↓Mg2+, ↓PO3-4 or ↓urea.
Management of alcohol withdrawal?
Monitor patients with significant alcohol history for withdrawal.
Prescribe reducing dose of chlordiazepoxide (benzo; correct electrolyte abnormalities; give vitamin replacements PO (thiamine 25mg/24h an vitamin B one tablet/24h) or IV (Pabrinex 2 pairs/8h IV for 5 days – a high-potency combination of B and C vitamins – may sometimes cause anaphylaxis).
Monitor BP and blood glucose.
Withdrawal seizures usually self-limiting.
3rd degree heart block history?
Asymptomatic, dizziness (+/- on standing), palpitations, shortness of breath, +/- chest pain.
3rd degree heart block examination?
↓BP (and potentially ↓GCS), cannon waves in ↑JVP (due to asynchronous contraction of right atria against closed tricuspid valve), signs of heart failure, features of underlying disease.
3rd degree heart block causes?
Underlying ischaemic damage (typically after inferior MI); also post cardiac surgery, drug induced (B-blockers, Ca2+ channel blockers), amyloid, saecoid, myeloma, infective (Chagas, Lyme).
3rd degree heart block investigations?
ECG – complete dissociation of P waves from QRS complexes; narrow QRS implies proximal lesion (may respond to atropine). Broad complex implies distal lesion (less likely to respond to atropine). Look for evidence of MI.
Bloods – FBC, U+E, Ca2+, Mg2+. TFT, cardiac markers, coagulation (if considering pacing wire)
CXR – unlikely to be helpful in immediate resuscitation phase.
Management of 3rd degree heart block?
If symptomatic (dizzy or GCS <15) or systolic <90mmHg…
- Monitor HR on defibrillator
- Lay flat with legs elevated
- O2 supplementation
- Secure IV access and take bloods.
- Call senior help/Arrest team
Titrate 500mcg atropine IV every 2-3 mins (max of 3mg), followed by large flush, until HR improves.
Identify and correct precipitant. Consider external pacing/pacing-wire via central line; a rhythmical precordial thump (percussion pacing) can be used in extremis when external pacing machine not available.
Complications of 3rd degree heart block?
Severe bradycardia and high vagal tone can deteriorate into asystole so prompt treatment required.
Remember to talk continuously to the patient and/or check for a pulse because pulseless electrical activity (PEA) is common and ECG trace may not change.
DKA history?
‘Osmotic symptoms’ – (thirst, polyuria, frequency, urgency) – tiredness, weight loss, vomiting, rashes, breathlessness, cough, sputum, chest pain, abdo pain, dysuria.
DKA examination?
Temp, RR, GCS, recent and current blood glucose, fluid balance.
Look for: volume status, sweet smelling breath (ketones).
DKA diagnosis criteria?
- Presence of hyperglycaemia (>11mmol/L)
- Acidosis (venous pH <7.3)
- Blood ketones >3mmol/L or ketonuria (>++)
DKA fluids?
0.9% saline is most appropriate in DKA.
In adults – 1L over 1 hour, another 1L over 2 hours, another 1L over 3 hours, another 1L over 4 hours.
Fluid challenge if SBP <90 – reassess frequently for signs of fluid overload.
DKA management?
ABCDE
- 15L/min O2 if SoB or sats <94%
- Call for senior help
- Establish venous access – take bloods.
FBC, U+E, glucose, osmolarity, HCO3-, blood cultures
- Check BP
- If SBP <90 – fluid challenge (0.9% saline), then recheck.
- If SBP <90, further fluid challenge and call ICU/critical care teams.
- If SBP >90, give 1L 0.9% saline IV over 60 mins.
- Check finger-prick glucose and ketones (dipstick urine for ketones if capillary testing unavailable).
- Start a fixed rate insulin infusion of 0.1 unit/kg/hr IV (use 50 units human soluble insulin e.g. Actrapid in 50ml 0.9% saline.
- VBG – if pH <7.1, call ICU/critical care team.
- Monitor glucose and ketones hourly, and venous HCO3-, K+ and pH at 60 min and 2 hourly thereafter; K+ will fall unless replaced.
Further management – ECG, CXR, MSU – to determine cause.
Reassess – ABCDE.
Continue insulin infusion until ketones<0.3mmol/L and pH >7.3. At this point convert to regular SC insulin if eating and drinking normally, otherwise using a sliding scale.
When to consider HDU admission in DKA?
Heart/renal failure
GCS <12, sats<92%
SBP <90
Young people, elderly, comorbities or pregnancy
Ketones >6mmol/L, HCO3- <5mmol/l, pH <7.1
K+ <3.5mmol/L, anion gap >16
What is HSS/HONK?
Severe, uncorrected hyperglycaemia leads to dehydration (volume depletion + haemoconcentration –> further increase in blood glucose level), but in the presence of residual insulin production in T2DM, ketoacidosis does not develop – (insulin inhibits hormone-sensitive lipase-mediated lipolysis).
Diagnostic criteria for HSS/HONK?
Raised plasma osmolarity (>340 mOsmol/kg) High glucose (>30mmol/L)
HSS/HONK history?
‘Osmotic symptoms’ – (thirst, polyuria, frequency, urgency) – tiredness, weight loss, vomiting, rashes, breathlessness, cough, sputum, chest pain, abdo pain, dysuria.
Life-threatening causes of HSS/HONK?
Insulin overdose, oral hypoglycaemia overdose, sepsis, alcohol excess, acute liver failure
Management of HSS/HONK?
ABCDE
- O2 15 L/min if SoB or sats <94%
- Call for senior help
- Establish venous access, take bloods:
FBC, U+E, glucose, osmolarity, blood cultures
- Give 1L 0.9% saline IV over 30 mins
- Check finger-prick glucose. Start a sliding scale if glucose still raised after 1h of fluids and potassium is sufficiently high.
- Monitor U+E and glucose
- Further management – ECG, CXR, MSU to determine cause
- Reassess – ABCDE
Continue IV fluid replacement (at half rate used in DKA) – over 24 hours.
Electrolyte replacement – severe potassium deficits.
Monitor U+E 2 hourly – hyperglycaemia will drive redistribution of water into extracellular fluid (intravascular), lowering serum Na+ concentrations (‘spurious hyponatraemia’).
Convert to insulin/oral hypoglycaemics when glucose <12mmol/L.
History for hypovolaemic shock?
Dizziness on standing (+/- lying), SoB +/- chest pain
Symptoms of underlying disease = trauma to chest, limb, abdo, pelvis, pain/melena/haematemasis, diarrhoea, frequency, epigastric pain to back, abdo swelling/bloating
Hypovolaemic shock examination?
BP <100mmHg systolic, ↑HR, weak/thready pulse, postural hypotension, cool peripheries/CRT >2s, ↓JVP, ↓GCS/restlessness, oliguria, mottled skin in severe hypotension
3 main causes of hypovolaemic shock?
Haemorrhage
Salt + water loss
3rd space loss
Investigations in hypovolaemic shock?
Bloods – FBC (↓Hb, may be normal early in acute blood loss), U+E (↑urea in GI bleed, ↓K+ in D+V), LFT, amylase, clotting, osmolalilty, cross-match
ABG – acidosis in haemorrhage, DKA and pancreatitis; alkalosis in vomiting
ECG – ischaemia
CXR - haemothorax
Pelvic X-ray – pelvic fracture
Abdo USS/CT – AAA (though if ruptured may need theatre before imaging) or free intra-abdominal fluid
Urine – Na+ and osmolality in diabetes insipidus
Stool – M, C + S
Classification of hypovolaemic shock - how much blood lost in each?
I - up to 750ml
II - 750-1500ml
III - 1500-2000ml
IV - >2000ml
Management of severe haemorrhage?
CALL SENIOR HELP
ABCDE
- Lay flat and elevate legs
- O2 15 L/min; IV access + take bloods
- 1L 0.9% saline STAT; attempt to stop bleeding by compression if appropriatel further 1L 0.9% saline STAT if no ↑BP or ↓HR
- Consider urgent blood transfusion (O -ve, type specific or full X-match)
- Identify likely cause of haemorrhage
- Seek involvement of surgeons/ICU
- Do not push systolic BP >100mmHg
- Monitor response
Pathophysiology of anaphylaxis?
Type I hypersensitivity reaction via IgE. Mast cell and basophil degranulation –> increased vascular permeability, bronchial smooth muscle contraction and myocardial dysfunction.
Sites of treatment = immunosuppression, anti-histamine, α and β(2) adrenoreceptor agonism,
Anaphylaxis history?
Chest tightness, wheeze, breathlessness, itching, swelling, anxiety/fear/agitation, GI disturbance (vomiting, abdominal pain, diarrhoea) – usually with 30 mins of exposure
Anaphylaxis examination?
Urticaria, bronchospasm/stridor, vomiting and/or diarrhoea, flushing, abdominal pain, sense of impending doom, hypotension, tachycardia, tongue/periorbital swelling, wheeze, cyanosis
Causes of anaphylaxis?
Drugs – penicillins, anaesthetic drugs, contrast media, blood products
Environmental – latex, stings, eggs, fish, strawberries, nuts
Management of anaphylaxis?
CALL FOR SENIOR HELP
ABCDE
- O2 15 L/min via NRBM
- IV access + bloods (if have time)
- Adrenaline 1:1000 solution 0.5mg (0.5ml) IM stat
- IV fluid 500-1000ml crystalloid
Hydrocortisone 200mg IV slowly
Chlorphenamine 10mg IV slowly
Salbutamol 5mg neb PRN
Consider referral to ICU
How do each of the management options in anaphylaxis work?
Adrenaline - vasoconstriction + reduces oedema (alpha) bronchodilation and increases CO (beta)
Hydrocortisone - prevents T cell proliferation
Chlorphenamine - inhibits vasodilation and bronchoconstriction
Salbutamol - bronchodilation
Examination in septic shock?
Fever, BP <100mgHg systolic, tachycardia +/- bounding pulse, warm peripheries, ↓JVP, ↓GCS, oliguria, mottled skin in severe hypotension
Cellulitis, non-blanching petechial rash (meningococcal septicaemia), chest creps (pneumonia), abdominal/loin/suprapubic tenderness (intra-abdominal infection)
Causes of septick shock?
Skin/soft tissues - cellulitis/gangrene Intra-abdominal perforation; biliary tract Chest pnuemonia Urinary tract UTI; pyelonephritis Heart endocarditis Post-op wound infection; bowel leak
What is the septic six?
Within 1st hour • Blood cultures (before administration of abx) • Urine output • Fluid resuscitation • Antibiotics (broad spec) • Lactate • Oxygen
Possible investigations in sepsis? (think about looking for source)
Bloods – FBC (↑WCC +/- ↓Hb), U+E, LFT, ↑CRP/ESR, glucose, clotting/fibrinogen, procalcitonin
Blood cultures – at least 2 sets from different sites, plus additional cultures from any central lines
ABG – acidosis, ↓BE, ↑lactate
ECG – ischaemia
Urine dipstick – blood, protein, nitrates, leucocytes, send for M, C + S
Erect CXR – consolidation, free air under diaphragm
Culture – skin/wound swabs, sputum
Echo – valvular lesion/vegetation if suspect endocarditis
Initial management of sepsis?
Call senior help
ABCDE
- Lay flat and elevate legs
- O2 15 L/min; IV access + take bloods
- 1L 0.9% saline STAT – repeat if no ↑BP or ↓HR – 30ml/kg crystalloid boluses until lactate <4mmol/L, systolic BP >90mmHg and MAP >65mmgHg
- Give IV abx appropriate to likely source of infection
- Consider central line to measure CVP and arterial line for serial ABGs an invasive BP monitoring
- Seek involvement of ICU as may need inotropic/ventilatory support
What to ask in head injury history?
Mechanism of injury, time of injury, loss of consciousness, seizures, memory (before, during and after), blood/fluid from nose or ears, vomiting, weakness/numbness/tingling in limbs, time of last meal, dizziness, visual changes, headache
Are they on anticoagulants?
Things to look for in head injury examination?
GCS, orientation, CSF leaking from ears (otorrhoea) or ears (rhinorrhoea), Battle’s sign (bruising over mastoid process; late sign), blood behind eardrum (haemotympanum), ‘panda’ eyes (bruising around eyes), focal neurology (e.g. weakness or numbness).
If head injury caused by fall, think about what precipitated fall (?dysrhythmia, hypoglycaemia, postural hypotension).
Obs in head injury?
GCS, HR, BP, RR, glucose
Initial management of head injury?
SENIOR HELP - bleep anaesthetist immediately if unconscious
ABCDE - follow NICE flowchart for CT
Indications for CT following head injury?
GCS <13 on assessment or <15 after 2 hours
Suspected skull fracture
Signs of basal skull fracture
Post-traumatic seziure
Focal neurological deficit
More than one episode of vomiting since injury
If none of these - are they on warfarin?
What is a subdural haematoma?
Venous bleed into skull; can be acute (↓GCS and ↑ICP, usually post-trauma) or chronic (fluctuating consciousness over days in e.g. elderly, alcoholics, patients on anticoagulation).
CT diagnosis; drained by craniotomy or burr hole.
What is an extradural haematoma?
Arterial bleed into skull often from middle meningeal artery after trauma.
Initially well but ↓GCS over 4-8h as blood collects.
CT diagnosis; drained by craniotomy or burr hole.
What is post-concussion syndrome?
Patients may have concussion symptoms for months after a head injury, e.g. headaches, tiredness, depression, memory problems.
Causes of seizure?
Most likely = idiopathic, epilepsy, alcohol withdrawal, hypoglycaemia, hypoxia, trauma.
Other = kidney or liver failure, pseudoseizures, overdose (tricyclics, phenothiazines, amphetamines)
Non-seizure = brief limb jerking during a faint, syncope, arrhythmias.
Life-threatening causes of seizure?
Hypoxia/cardiac disease Hypoglycaemia Metabolic (↓Ca2+, ↑Na+) Trauma Meningitis, encephalitis, malaria ↑ICP and CVA Drug overdose Hypertension/eclampsia
Investigations in seizure?
Bloods – FBC, U+E, LFT, glucose, Ca2+, Mg2+, blood cultures, anticonvulsant levels.
ABG – if hypoxia or metabolic upset suspected
Urine – consider drug screen,
β-hCG if pre-menopausal and female.
ECG – to exclude dysrhythmia
CT – may show a focal lesion, ↑ICP, haemorrhage or infarction. Perform as urgent if the patient has a persistent GCS <15 post-fit, focal neurology or if seizure was <4d post trauma
MRI – is neuroimaging of choice in suspected epilepsy
LP – if meningitis or encephalitis suspected
EEG – may help to exclude encephalitis or as out-patient investigation for epilepsy
General management of seizures?
ABCDE
- If no respiratory effort/no palpable pulse – call arrest team
- If GCS <8 – call anaesthetist
Call for senior help if seizure >5 min. All timings from start of first fit; clock only restarts once patient has been fit free for >30 mins.
Stop the seizure using below pathway. Correct any metabolic upset (glucose, Mg2+, Ca2+, Na+) and exclude life-threatening causes whilst trying to establish cause. Secure airway if still fitting or GCS <8.
Initial management of seizure? (0-5 mins)
- Start timing
- 15 L/min O2 via NRBM
- Keep patient safe and put into recovery position if possible
- Monitor HR, O2, sats, BP, cardiac trace, temp * Venous access (after 3-4 minutes) – take bloods o FBC, U+E, LFT, Ca2+, glucose, blood cultures, anticonvulsant levels.
- Check glucose: if <3.5mmol/L give 100ml of 20% glucose STAT
Management of seizure? (5-20 mins)
- Call for senior help and attach cardiac monitor
- Consider airway adjunct but do not force teeth apart
- If IV access: lorazepam 4mg IV over 2 min, repeat at 10 min if no effect
- If no IV access: diazepam 10mg PR, repeat every 10min if no effect up to 30mg total
- Ask ward staff about history/check notes
- If alcoholism/ malnourished give Parbinex 2 pairs IV over 10min if not already given this admission
Causes of stroke?
Ischaemia – 85% - AF, carotid stenosis
Haemorrhage – 15%
Territories of stroke
Posterior Circulation Strokes (POCS) Affect territory of verterbrobasilar artery (occipital lobes, brainstem + cerebellum)
Anterior Circulation Strokes (TACS, PACS, LACS) Internal carotid artery territory, which supplies all the rest of the brain.
What is a TACS?
All of:
- Motor/sensory deficit in 2 or more of face, arm or leg
- Homonymous hemianopia
- Higher cortical function
What is a PACS?
Either * 2 out of 3 of TACS criteria met Or * Higher cortical dysfunction alone Or * Isolated motor deficit not meeting LACS criteria
What is a LACS?
Motor and/or sensory deficit affecting 2 or more of face, arm, leg No higher cortical dysfunction or hemianopia
What is a POCS?
Any of:
- Ipsilateral cranial nerve palsy + contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Disordered conjugate eye movement
- Cerebellar dysfunction
- Isolated hemianopia or cortical blindness
Investigations in suspected stroke?
Bloods – Acute - FBC, U+E, LFT, lipids, glucose, cardiac markers, clotting, G+S
ECG
CXR
CT head – urgent if within thrombolysis window, GCS persistently low, on oral anticoagulants/known bleeding disorder, severe headache at onset of stroke or evidence of ↑ICP; otherwise within 24h.
Echo/carotid Doppler/24h ECG – if anterior circulation stroke.
Initial management of stroke?
Call for senior help ABCDE
- 15 L/min O2 via NRBM * Monitor O2 sats, RR, HR, cardiac trace, temp and BP
- Venous access + take bloods (FBC, ESR, U+E, LFT, lipids, glucose, cardiac markers, clotting, G+S)
- NBM + start IV fluids for hydration (0.9% saline at 100ml/h)
- ECG looking for atrial fibrillation/arrhythmia
- Take a focused history * Examine the patient (RS, CVS, abdo + neuro exam – document exact neurological deficits).
- Request urgent CT scan
- Consider thrombolysis OR aspirin 300mg PO STAT after CT excludes haemorrhage
- Reassess - ABCDE
Indications for thrombolysis
- Age <80 - <4.5 hours from start of symptoms
- Age >80 - <3 hours from start of symptoms
- Non-haemorrhagic stroke (excluded by CT)
- Significant symptoms and not improving
Contraindications to thrombolysis?
Active bleeding, CNS trauma, neoplasms or arteriovenous malformations, previous intracerebral haemorrhage, ischaemic stroke in previous 6mths, major trauma/surgery in past 3wk, non-compressible punctures in past 24hrs (LP etc).
Further management of stroke?
- If no thrombolysis – aspirin 300mg/24h PO/PR for 14d (provided no haemorrhage on CT)
- Assess safety of swallow; if concerns, keep NBM + IV fluids and request SALT assessment.
- Admit to stroke ward for early mobilisation and rehabilitation with multidisciplinary team.
Subarachnoid history and examination?
History - Rapid onset (<2 min), severe, continuous (>2h) headache; often occipital (‘hit around back of head’), vomiting, dizziness; may have had seizures.
Exam - Neck stiffness, drowsy, photophobia, focal neurology, ↓GCS
Subarachnoid investigations?
CT Head – URGENT
LP – (>12 hours after onset) - if CT normal, as CT may miss small bleeds. Looking for xanthochromia
Subarachnoid management?
15 L/min O2
Analgesia (codeine 30mg PO or 5mg morphine IV) and anti-emetic (metoclopramide 10mg IV/IM).
Refer urgently to neurosurgeon for endovascular coiling or neurosurgical clipping and consider transfer to ICU if ↓GCS.
Lie patient flat and advise not to get up or eat.
Reassess often and request neuro obs.
Nimodipine (60mg/4h PO) prevents vasospasm and improves outcome.
Keep systolic <130mmHg, using IV β-blockers, unless lethargic (suggests vasospasm; may require permissive hypertension).
