Emergency Flashcards
HAEMORRHAGE
i) what four things can constitute major haemorrhage? what are the seven steps in major haemorrhage mx?
ii) what is the first step in mx if major trauma? name three drugs that can be used
iii) what type of access should be obtained? name three bloods that should be taken? what should be done in shock/traumatic brain injury? why? what should not be used if active bleeding? what should be given instead
iv) what is given if red cells are falling? if PT ratio is >1.5? if fibrinogen is <1.5 and if plats are <75? name there scans that may be done if non responsive? what scan can be done if they are responding to resus or HD stable? what scan should not be used before CT/to determine whether they need CT?
v) what should be used to control external haemorrhage? what can be done if there is major limb trauma? what protocol is started if the patient is actively bleeding? what test can determine if its a bleeding or clotting problem?
i) Major haemm = loss of more than one blood volume in 24hrs (>5L in 70kg adult) or 50% of total blood vol loss in 3hrs or Bleeding in excess of 150ml/min or systolic BP <90 with HR >110bpm
1) reverse anti coag, 2) circ access and fluid replace, 3) dx imaging, 4) dressing and tornuquet, 5) haemorrhage protocol, 6) haemostatic agents, 7) surgery and IR
ii) reverse anti coags > don’t use vitamin K (take too long)
- pro thrombin complex can instantly reverse warfarin > provides coag factors or adnexanet alfa to reverse factor Xa inhibitors - only reverse in life threatening/uncontrolled bleeding
iii) circulatory access and fluid replace - use peripheral IV access or IO if IV fails while central access is being inserted
- take baseline bloods before transfusion for FBC, G&S, clotting (inc fibriogen)
- If shock and traumatic brain iniry > restrictive volume resus if shock or less restrictive vol resus if TBI to maintain ceb perfusion
- Dont use crystalloids if active bleeding (use plasma and RBC to replace volume)
- Use O neg until blood group is known
If bleeding continues > give further FFP 1L (4 units) per 6 units red cells, consider cryoppt, consider plats
iv) If falling Hb > red cells
PT ratio >1,5 > FFP
Fibrinogen <1.5 > cryoppt 2 pools
Plats <75 > give plats
- Dx imaging in hopsital > Limit to min needed eg chest/pelvis Xray, FAST scan if unstable
- Negative fast scan does exclude retro or intraperitoneal haemm
- Immed CT if they are responding to resus or are haemodynamically normal
- Don’t use FAST (focus ass sonography for trauma) scan before CT or to determine whether they need CT
iv) Dressing and torniquets > use simple dressing with direct pressure control to control ext haemm
- if major limb trauma > use tornuquet if direct pressure has failed
- If active bleeding > start with fixed ratio protocol for blood components > then change to lab guided coag
- Viscoelastometric POC testing eg ROTEM > determine whether its a bleeding or clotting problem
HAEMORRHAGE TREATMENT
i) what haemostatic agent should be used ASAP with major trauma/active bleeding? within what time period is this given?
ii) what type of surgery is done for patients that are unstable and not responding to volume resus? what is done if they are responding to resus?
iii) what is done for active arterial pelvic haemorrhage? what can be done for patients with blunt thoracic injury?
iv) what causes 35% of upper GI bleeds? which source has the highest mortality? what is done for initial resus? name two things that can be used to reverse warfarin in this case? what are the risks of over transfusion?
i) Haemostatic agents > use IV tranexamic acid ASAP with major trauma and active bleeding
Dont use IV TA >3hrs most injury unless hyperfibrinolysis
ii) damage control sx in haemodynam unstable pts that arent responding to volume resus
- Definitive sx if haemodynaic unstable but are responding to vol resus or HD normal
iii) IR for active arterial pelvic haemmorhage unless immed open sx is needed for other reasons
- Joint IR and sx for arterial haemmorhage that extends to sx inaccessible regions
- endovasc stent graft for patients with blunt thoracic injury
iv) Acute upper GI bleed > 35% caused by pepic ulcer
- Highest mortality from those presenting with oes or gastric varices
- Initial resus > transfusion of red cells, plats, clotting factors
- Use IV vit K or prothrombin complex conc to reverse warfarin
- If HD stable or bleeding less sereve > over transfusion can increase bleeding and risk of mortality
THE ACUTE ABDOMEN
i) how is it characterised? what does initial assessment aim to do? what question do you first need to ask?
ii) name three differentials for pain in - RUQ, RLQ, LLQ, LUQ, epigastric, periumbilical?
iii) name three presentations that warrants urgent intervention?
i) sudden onset severe abdo pain dev over a short period of time
- initial asess > determine if pt has an acute sx problem or medical therapy
- is the patient critcally unwell? 10 second assess of clinical state > end of bed and obvs
ii) RUQ - cholecystsitis, pyelonephritis, ureteric colic, hepatitis, pneumonia
- RLQ - appendicitis, ureteric colic, IBD, UTI, gynae, testic torsion
- LUQ - gastric ulcer, pyeloneph, ureteric colic, pneumonia
- LLQ - diverticultiis, ur colic, inguinal hernia, IBD, UTI, gynae, testic torision
- epigastric - PUD, cholecytsitis, pancreatitis, MI
- peri umbilical -small/large bowel obstruc, appendicitis, AAA
iii) bleeding, perforated vicus and ischaemic bowel
THE ACUTE ABDOMEN
i) name three causes of bleeding? what complication may these patient have?
ii) what does a perforated viscus present with? name three things that can cause it? how will a patient with generalised peritonitis act? how does this differ from renal colic? name four other signs
iii) how does ischaemic bowel present? what two things may be seen on ABG? what is the definitive dx?
iv) how does colicky pain present? what is peritonism? what is it usually due to? why does pain migrate in acute appendicitis?
i) Bleeding - intra abdo (ruptured AAA) > refer to vasc
- other bleeding - ruptured ectopic, gastric ulcer, trauma
- pts will go into hypovol shock > tachycardia and hypotension, pale and clammy, cool to touch
ii) Perforated viscus > peritonitis
- generalised peritonitis is commonly due to perforation of abdo viscus
- perf - peptic ulceration, S/LB obstruction, diverticular disease and IBD
* generalised peri - lay completely still, look unwell (renal colic constant move and cant get comfy)
- signs of tachy, hypotension, rigid abdo with percussion tender, invol guarding, reduced/absent BS (ileus)
iii) Ischaemic bowel
- pain out of proportion with clinical signs - IB untill proven otherwise
- acidaemic, raised lactate and physiol compromised
- diffuse and constant pain, exam can be unremarkable
- definitive dx with CT scan with IV contrast
iv) colic - crescendo pain > severe then goes away due to biliary, ureteric, bowel obstruction
- Peritonism - localised inflam of peritoneum (not peritonitis)
- usually due to inflam of a viscus that irritates visc then parietal peritoneum > abdo pain starts in one place (visc) then localised to another area (parietal)
- happens in acute appendicitis > pain migrates from umbilical region to RIF
ACUTE ABDOMEN - INVESTIGATIONS AND TX
i) name three bedside tests that may be done? when would you do an ABG? what does raised lactate indicate?
ii) which routine bloods should be done? (5) name three imaging that may be done?
iii) what does tx depend on? name five things all patients should get? what should unwell patients be considered for? (2) what should be monitored?
i) urine dip - infection or haematuria > send MC&S and pregnancy test
- ABG - bleeding or septic patients (lactate = tissue hypoperfus)
* routine bloods - FBC, UE, CRP, amylase, G&S
ii) Imaging - erect CXR for free abdo air
- US - KUB for hydroneph, bil tree and liver for gallstones, GB thickening or duct dilatation, transvaginal for tubo ovarian pathology
CT abdo
ECG
iii) Depends on cause
IV access, NBM, analgesia, anti emetics, imaging, VTE prophylaxis, urine dip, bloods
* if unwell > catheter or NG tube
* Start IV fluid and monitor fluid balance
CARDIOPULMONARY ARREST
i) how quickly should CPR be started? how many breaths:compressions? how many compressions per minute? depth of compression? what must there be time for?
ii) what is CP arrest? what is the most common cause? what is the most common mechanism? what is seen in 80% of cases post mortem?
iii) name four cardiac causes? name three resp causes? name three possible preceeding symptoms?
iv) should CPR be interrupted for bloods or radiol? what can be used to evaluate heart activity?
i) CPR: start within 10s
2 breaths after 30 compressions
100-120 compressions per minute
2-2.4 inches depth of compress
Give time for chest recoil
ii) Cessation of adequate heart function and respiration > death without reversal
- often occ in coronary artery disease
- most commonly caused by a primary cardiac event > most common mech is VF (can also be pulseness electrical activity and asystole)
- 80% post morterm have CAD with extensive athero
iii) Cardiac causes - 50-60%
* coronary artery disease, MI, myocardial hypertrophy, valvular heart disease, dilated CM, inherited disorders, HF, congenital (TOF)
- Resp causes
* airway obstruc, PE, resp muscle weakness due to spinal cord injury
- preceding symptoms - palpitations, SOB, nausea, chest pain
iv) Don’t interrupt CPR for bloods or radiology
* can do point of care testing eg blood glucose/K+ if it doesn’t interfere
* can use POC US during CPR to evaluate heart activity
MANAGEMENT OF CP ARREST
i) what is the first stage? what should be looked at? (4) what can be done to keep the airway patent? (2) name three signs of foreign body in resp tract?
ii) what is the second step? what is the third step? name two medications that may be given? name four things that are monitored in ALS? what may be inserted?
iii) what does post resus care start with? what is patient outcome determined by? what can be done for longterm mx? what is done if myocardial ischaemia was the cause?
iv) what is given after failed defib? when can this be repeated? what is done after 2-3 failed attempts at defib? (2) what drug can be given?
v) name four other complications of CP arrest?
i) initial evaluation with BLS
- look at conc, skin colour, breathing, arterial pulse
- look for foreign body in resp tract = stridor, dyspnoea, interctsal recession
- keep airway patent - head tilt, OP/NP
ii) defibrillation
- 3) ALS
- do BLS, airway mx and meds such as adrenaline and amioadarone
- ALS = adequate ventilation, stab BP, CO, control arrhythmia and restore organ perfusion
- defib/pacing, endotrach tube/mech vent, IV line insertion
iii) post resus care
*starts with return of spontaneous circulation
* pt outcome is determine by haemodynamic stability (instab = asystole, bradyarrhy, pEA)
- long term management > if survive with no brain damagre > investigate cause and prevent in the future
- if cause if myocardial isch > manage surgically
iv) After failed defib > give adrenaline 1mgIV > can repaeat after 3-5 mins
- 2-3 failed attempts > immed intubate and ABG
- Can give anti arrhythmics eg amiodarone after electrical instab and failed defib
v) pneumothorax, haemothorax, lung laceration, pulm haemmorage, cardiac tamponade
EXTRA DURAL HAEMORRHAGE
i) what is it? which sex has higher incidence? which age? what does it usually occur due to?
ii) what is the most common type of fracture? what artery is most common cause of bleeding? why? name two other causes
iii) what does a patient usually present with a history of? what happens in relation to LOC? name three other symptoms? what clinical features may be seen? what happens if its left untreated?
iv) what guidelines should be used to manage? which bloods should be done urgently? (5) what will CT classically show?
i) extra axial (outside the brain) bleed that occurs between the dura and skull bone
- incidence higher in men 20-30yrs old (assoc with high risk behavs - crime and contact sport)
- usually occurs due to blunt force head trauma > linear skull fracture with min/no displace
ii) parieto temporal fractures are most common due to RTA
- middle meningeal artery is most common cause of bleeding > fracture pterion > lacerates anterior branch of MMA that runs underneath
- can also be caused by diploic vein bleeds, vascular malformations or infective pathology
iii) History of trauma or fall
* initial LOC then lucid period then further deteriorate
* headache, nausea, vomiting, progressive drowsy
* low conc level, localising neurol signs
* clinical features of brain herniation or raised ICP
* untreated > coma and death
iv) Manage as per ATLS guidelines (adv trauma life support)
* routine urgent bloods - FBC, UE, CRP, clotting, G&S
* CT head > classically shows hyperdense bioconvex lesion (lens shaped) can also be assoc with a skull fracture
EXTRA DURAL HAEMORRHAGE MANAGEMENT
i) what guidelines are used to manage? what should be done once stable? over what volume should always be surgically managed?
ii) name four features that do not need surgical mx and can be managed conservatively? what does cons manage involve? (2)
iii) which surgical procedure shows definitive benefit? name two procedures that may be done? what can be done once source of bleeding is identified? (2) name three things that can be done post op?
iv) what is overall mortality? name four things that suggest a poor prognosis?
i) manage with ATS
* once stable > urgent neurosurgical opinion
* not all require surgery
ii) >30cm3 always surgically manage
* <30cm3 with low thickness, minimal midline shift and GCS >8 without focal neurol deficit > conservative mx
- Conservative mx > serial CT imaging and close neurol observation
iii) no specific sx procdure shows definitive benefit may do cranitotomy or burr holes
* identify bleeding source > control throigh ligation or cauterisation
* post op > neuro critical care or HDU, routine CT scans and neurorehab
iv) Overall mort is 30%
- poor prognosis > increasing age, temporal location, low GCS at presentation, herniation or increased ICP
SUB ARACHNOID HAEMORRHAGE
i) where do you bleed into? what causes 85% of cases? name three things this can be associated with? name three things associated with the remainder of cases?
ii) what age is it common in? what type of pathology is it often caused by? name three risk factors?
iii) what is the common presenting symptom? name four other symptoms? what may examination show?
i) bleeding into sub sarach space (between arach and pia)
* aneurysmal (85%) > assoc with AD polycystic kidney dosease, fibromusc dysplasia, conn tissue disorders, athero and HTN
* non aneurysmal - trauma, arteriovenous malforms, coagulopathies
ii) occ in patients around 60yrs old
* can be caused by berry aneurysm rupture (occ at bifurcation of arteries - MCA in COW)
* RF - FH, female, african descent
iii) severe headache, sudden onset in occipital region (thunderclap)
- nausea, vomiting, reduced conc, collapse, seizure, meningism (photpphobia, stiff neck, pain on neck flexion)
- exam may show focal neurology, meningism
SUBARACHOID HAEMORRHAGE
i) what urgent imaging should be done? what will be seen? (2) what is done if imaging is negative but there is clinical suspic? what will be seen if SAH?
ii) once SAH is confirmed what should be done? what is the mainstay of treatment?
iii) what should initial treatment involve? (3) which drug can be given to reduce vasospasm and reduce delayed ceb ischaemia?
iv) what warrants surgical intervention? what two surgical approaches can be done? what does this depend on? (3) what makes up the majority of surgical approaches?
v) name three complications? what can be given prophylactically to reduce seizure risk?
i) Confirm presence then localise the source
* urgent non contrast CT head > hyperattenuating material in SA space most typically around COW or lateral sulcus
* if CT head neg but clinical suspicion > do LP > see elevated levels of oxyHb and bilirubin in CSF in SAH
ii) once SAH confirmed > do definitive imaging to localise source of bleed > CT angiography, digital subtraction angiography (vis of small vessels and feeding vessels)
- Mainstay is definitively treat the bleeding region and reduce potential complications
iii) A-E with fluid resus, analgesia, anti emetics
* early neurosurgical involvement
* start patients on nimodpine (CCB that can reduce vasospasm and reduce risk of delayed ceb ischaemia)
iii) Surgical mx
* rupture aneursym SAH require sx intervention > coil or clip it dep on location, size, age, comorbids
* 80% aneurysms are coiled > more suited if multi co morbids, older patient age, pres of vasospasm, aneurysms deep or along basilar artery
* clipping only really done if morphology isnt suited to coling, if there is a clot or a prev coiled anuerysm has ruptured
v) Rebleeding, hydrocephalus, vasospasm, electrolyte disturbance (hyponat)
* may give prophylactic leviteracitam to reduce seziure risk
SUBDURAL HAEMORRHAGE
i) what is it? what is classed as acute, sub acute and chronic? what is simple or complicated? what causes it? what type of injury?
ii) what happens after the injury? what can this lead to if untreated? name four risk factors? why are older people more vulneravle to SDH?
iii) how may patient present (4) what should always be looked for in children? what will affect how it appears on CT? how will acute, sub acute, chronic appear on CT?
iv) name four routine bloods that should be done? what is gold standard imaging? what shape will the area of abnorm be? what feature may also be present?
i) collection of blood in the subdural space between dura and arachnoid
* acute (<3d post injury), subacute (3-21d) or chronic (>21d post injury)
* simple = no parenchymal injury or complicated
* occ from tearing of the bridging veins that cross from the cortex to dural venous sinuses > vulnerable to deceleration injury
ii) get accum of blood between dura and arach > gradual rise in ICP > hernation and bs death if untreated
- RF = trauma, increasing age, ETOH excess/epilepsy (prone to head injury/fall), clotting disorder, on anti coag
- bridging veins more vulnerable at older age due to brain atrophy > stretching of the veins
iii) altered level of conciousness, headaches, focal neurology, raised ICP (blurry vision, worse headache), seizure activity
* acute SDH features occur quickly but chronic = latent period of weeks/months
* initial injury may not be noticed or forgotten espec if old/ETOH
* in children always look for non accidental injury
* will appear different on CT dep on time of presentation - acute = diffusely hyperdense (light), subacute = hetro hyperdense or isodense, chronic = diffusely hypodense (dark)
* acute on chronic > areas of hyperdensity and hypodensity
iv) outine bloods - FBC, CRP, UE, LFT and clotting, G&S
* gold standard imaging is non contrast head CT > crescent shaped collection of blood over one hemi
* with or without midline shift
SUBDURAL HAEMORRHAGE TREATMENT
i) what should be managed first? what needs to be reversed? what is definitive mx based on?
ii) when may a patient be conservatively managed? name two indications for surgery? what two procedures may be done for acute SDH?
iii) what surgical procedure may be done for chronic SDH?
iv) name four complications of SDH? what is there increased risk of?
i) manage raised ICP
* reverse anti coag
* if fall > investigate for underlying reason
* definitive mx based on size/clinical features
ii) conservative mx for small acute that don’t cause ML shift, no neurol deficit
* acute SDH that need surgery > trauma craniotomy with hemi craniectomy if sigfic cerebral swelling/assoc contusions
iii) chronic SDH - burr hole craniotomy (drill holes in skull to allow blood to drain) with irrigation or twist drill cranotomy with drain placement
iv) cerebral oedema
* raised ICP, seizures, herniation, persis veg state, permanent neuro deficits
* increased risk of recurrent haematoma formation folllowing initial SDH
NECROTISING FASCITIS
i) what is it? what type occurs in the perineum? what causes type I? what causes type II? name four risk factors?
ii) which bacteria can cause gas gangrene? what is seen in GG?
iii) what may be seen in some patients on presentation? what type of pain is seen? what may be normal in early stages? name three things that happens as it progresses?
iv) name four late signs? what will be raised on bloods? what may be seen on ABG (2) is imaging routine? what risk score is used? name four things the risk score includes?
i) life threatening, rapid progressing infection > fascial planes and sub cut tissue
* high mortality (up to 40%) and is a surgical emergency
* fourneriers gangrene is a spec type in the perineum
- Type I - polymicrobial infection caused by a mix on anerobes (bacteroides) and aerobes (s aureus) - more common subtype and espec in elderly and co morbid patients
- Type II - monomicrobialcaused by strep pyogenes (group A strep_ and more common in healthy people with hx of trauma
* RF - DM, CKD, ETOH excess, adv age or frailty, malnutrition, met cancaner or immunocomp
ii) gas gangrene is a form of NF caused by clostridium specifies > gas produced by vacteria within the tissue > large bullae of gas in infected tissue and tissue crepitus is present on light palpation (crackling)
iii) some may have recognised ppt event of skin breach (sx, trauma, bite)
* clin features progress rapidly > severe pain out of proportion with clinical signs
* HD unstable, multi organ dysfunction
* exam signs are varied > overlying skin can be normal in early stages
* progression > skin erythema, oedema, skin ischaemia
iv) late signs = skin crepitus, vesicles, bullae and obv skin necrosis
Bloods > raised WCC and CRP
* blood gas - raised lactate with or without metabolic acidosis
* signs of worsening renal function, hyponat, impaired liver function, raised glucose, coagulopathy
* imaging is not routine
- Risk score > laboratory risk indicator for nec fasc <5 is low risk, 6-7 intermed and >8 high risk (includes Hb, WCC, sodium, creatinine, glucose, CRP)
NECROTISING FASCITIS TX
i) what needs to be done immediately (2) name three things that should be given? how is area affected recorded?
ii) which department should have early input? what is the only definitive management?
iii) what needs to be done surgically first? what happens 24-48hrs later? what may be needed after initial infection has been cleared?
i) surgical emergency > imemd resus and debridement
* urgent broad spec abx, resus with IV fluids and catheterisation
* redness/discolour needs to be marked and time denoted
ii) early ITU input
- Surgical is only definitive mx
iii) first need urgent surgical debridement, excise any necrotic tissue until only viable bleeding tissue is present
* pack post debride and re look in 24-48hrs to check for evidence of inrection or further necrosis > may need further debridements
* post op > HDU or ITU
* may need reconstructive tx after initial debride and infection cleared > skin grafts or flaps (plastics)
