Emergency Med Flashcards
Causes of epistaxis
Local trauma: Nose picking, Facial trauma, Foreign bodies, Nasal or sinus infections, Nasal septum deviation
Dry/cold conditions, Prolonged inhalation of dry air (oxygen), Iatrogenic
NG tube insertion, Nasotracheal intubation, Medicinal
Topical corticosteroids and antihistamines Solvent inhalation Snorting cocaine Anticoagulants Coagulopathic
Inherited coagulopathies Splenomegaly Platelet disorders Chronic alcohol abuse AIDS Vascular abnormalities
AV malformation
Hereditary haemorrhagic telangiectasia
Endometriosis
Epitsaxis mangement
NB commonly occurs to ‘Little’s area’
- Pressure (apply to anterior soft part, 15-20min, sit forward to avoid blood dripping posteriorly; this controls 90% of nosebleeds)
- Cautery (only on one side of septum to avoid perforation, use silver nitrate only if you can see site of bleeding)
- Anterior packing using Rapid Rhino for 24hrs (nasal tampon with carboxycellulose coat which promotes platelet aggregation, with an inflatable balloon, insert in both nostrils to tamponade)
- Foley Catheter via nose into oropharynx and inflate gently.
Retrophargyngeal air
Air within the retropharyngeal space and tracking anteriorly along other neck fascial planes. The cause of the air leak may be a local perforation of the upper aerodigestive tract or the air may have tracked from the chest such as may be seen in pneumomediastinum related to asthma or with oesophageal perforation. Clinical correlation and chest x-ray would be useful for further clarification. Contrast swallow under fluoroscopy could be used to exclude a pharyngeal or oesophageal leak if required.
Surgical emphysema
Surgical emphysema (or subcutaneous emphysema) occurs when air/gas is located in the subcutaneous tissues (the layer under the skin). This usually occurs in the chest, face or neck. Clinically it is felt as crepitus and, if extensive, may cause soft tissue swelling and discomfort. Even when severe, subcutaneous emphysema is typically benign, although complications such as airway compromise, respiratory failure, pacemaker malfunction and tension phenomena have been described.
In the trauma situation, the gas often does not need treatment itself, but its importance lies in the fact that its presence indicates possible serious injuries that do require urgent management.
Causes can be divided into external and internal causes:
Internal - oesophageal perforation, pneumothorax, pneumomediastinum, interstitial emphysema
External - trauma e.g. fractured rib, post surgery/chest drain insertion (iatrogenic)
What is Charcot’s foot?
Rare, devastating complication of diabetes.
Neuro-inflammatory condition that occurs in a minority of patients with diabetes, and may lead to collapse of the longitudinal and transverse arches of the foot.
Pain, erythema, and redness may appear acutely, mimicking a foot infection. Chronic deformation may lead to repetitive trauma of the mid-foot (arch) during walking, leading to ulceration in this area.
Management is challenging and may require specialized orthopedic reconstruction to prevent or treat limb-threatening foot infections.
On XR the 5 Ds are signs:
Density change (areas of lucency and sclerosis)
Destruction
Debris (loose bodies and bone fragments)
Distension (joint effusion)
Dislocation (e.g. metacarpophalangeal joints).
What is gas gangrene?
When there is extensive air present in the soft tissues of (gas-gangrene) – it is likely to relate to infection with a gas forming organism e.g. Clostridium perfringes, following trauma.
Gas gangrene is pervasive and difficult to treat. A combination of broad-spectrum IV antibiotics and surgical debridement is often required to eradicate and prevent rapid spread through soft tissues. A typical antibiotic regime should cover gram positive, gram negative and anaerobes such as tazocin + clindamycin.
DM is a risk factor.
Sepsis management (acute)
Blood tests: Serial ABGS, or VBGS for lactate; blood cultures; U&E, CRP,
FBC, LFT, clotting screen
Micro samples: Sputum and urine for MC&S; swab any wounds; consider
LP; send fluid from drains and lines; joint aspirates; ascitic tap
Imaging: CXR, consider CT/USS/MRI/echo of suspected source
Antibiotics: These should be broad spectrum and start within 1h. Consider covering for non-bacterial microbes, eg give aciclovir if HSV encephalitis is suspected.
Fluids: Give within 1h if high risk with SBP <90, AKI, or lactate >2 (consider if <2).
• Give 500mL boluses of crystalloids with 130–154mmol/L sodium (eg 0.9% saline)
over 15mins. Caution in heart failure.
• If no improvement after two boluses, speak with a senior.
Oxygen: Give oxygen as required for target saturations. These will be 94–98% (or 88–92% if the patient is at risk of CO2 retention, eg in severe COPD).
Critical care review: Speak with critical care early if intensive care support (eg
inotropes, ventilation, haemofi ltration, intensive monitoring) may be required.
Surgical involvement: Eg emergency wound debridement.
Manage acute complications: Shock, AKI (p298), DIC (p352), ARDS (p186), arrhythmias (may spontaneously resolve when sepsis improves)
Assessing risk in sepsis (i.e. after diagnosis)
High risk- Request immediate senior review
Moderate- high - clinical review iwthin 1 hr, senior review w/in 3 if cause not identified
High risk criterion (1 of these):
- Altered mental state
- RR >24
- SBP < 90 or >40 less than baseline
- HR >130
- UO nil for 18hr or <0.5ml/kg/h if catheterised
- Mottled ashen or cyatnoic skin., non blanching rash
Or 2 moderate risk factors + lactate >2 or AKI (not listed here)
Anaphylaxis mimics
- Carcinoid
- Phaeochromocytoma .
- Systemic mastocytosis.
- Hereditary angioedema.
Anaphylaxis managment
- Secure the airway—give 100% O2
Intubate if respiratory obstruction imminent - Give adrenaline IM 0.5mg (ie 0.5mL of 1:1000). Repeat every 5min, if needed as guided by BP, pulse,
and respiratory function, until better. Adrenaline is given IM and NOT IV unless the patient is severely ill, or has no pulse. The IV dose is different: 100mcg/min—titrating with the response. This is 0.5mL of 1 : 10 000 solution IV per minute. Stop as soon as a response has been obtained. - Secure IV access and give Chlorphenamine 10mg IV and
hydrocortisone 200mg IV - IVI (0.9% saline, eg 500mL over ¼h; up to 2L may be needed) Titrate against blood pressure
- If still hypotensive, admission to ICU and an IVI of adrenaline may be needed ± aminophylline (p811) and nebulized salbutamol (p811): get expert help
Further Management:
• Admit to ward. Monitor ECG
• Measure serum tryptase 1–6h after suspected anaphylaxis
• Continue chlorphenamine 4mg/6h PO if itching
• Suggest a ‘MedicAlert’ bracelet naming the culprit allergen
• Teach about self-injected adrenaline (eg 0.3mg, Epipen®) to prevent a fatal attack
• Skin-prick tests showing specifi c IgE help identify allergens to avoid
STEMI
- Attach a ECG 12 lead
- IV access - bloods for U&E, glucose, troponins
- Brief assessment (Risk factors, exam, BP, JVP, mumur, CCF signs, scars, any drug history that is CI to PCII)
- Aspirin 300mg unless given already. Ticagrelor 180mg (or alternative antiplatelet)
- Morphine 5-10mg + anti-emetic e.g. metoclopramide 10mg IV
- STEMI confirmed on ECG and PCI available within 120 min
- Yes: Primary PCI
- No: Fibrinolysis (Transfer to primary PCI
centre for either rescue PCI if fibrinolysis unsuccessful or for angiography)
Patients with STEMI who do not receive reperfusion (eg presenting >12h after
symptom onset) should be treated with fondaparinux, or enoxaparin/unfractionated
heparin if not available.
RV infarction
Confirm by demonstrating ST elevation in rV3/4 and/or echo. NB: rV4 means that V4 is placed in the right 5th intercostal space in the midclavicular line. Treat hypotension and oliguria with fl uids (avoid nitrates and diuretics).
Monitor BP carefully, and assess early signs of pulmonary oedema. Intensive
monitoring and inotropes may be useful in some patients
Reperfusion therapy
Look for typical clinical symptoms of MI plus ECG criteria:
• ST elevation >1mm in ≥2 adjacent limb leads or >2mm in ≥2 adjacent chest leads.
• LBBB (unless known to have LBBB previously).
• Posterior changes: deep ST depression and tall R waves in leads V1 to V3.
Therapy may be percutaneous intervention (PCI—with angiographic identification of the culprit blockage(s) and revascularization via deployment of an expandable metal stent) or thrombolysis (with systemically administered clot-dissolving enzymes)
Primary PCI
Should be offered to all patients presenting within 12h of symptom
onset with a STEMI who either are at or can be transferred to a primary PCI centre
within 120min of first medical contact. If this is not possible, patients should
receive thrombolysis and be transferred to a primary PCI centre after the infusion
for either rescue PCI (if residual ST elevation) or angiography (if successful). Use beyond 12h if evidence of ongoing ischaemia or in stable patients presenting after 12–24h may be appropriate—seek specialist advice.
Thrombolysis
Benefit reduces steadily from onset of pain, target time is <30min from admission; use >12h from symptom onset requires specialist advice. - Do not thrombolyse ST depression alone, T-wave inversion alone, or normal ECG. Thrombolysis is best achieved with tissue plasminogen activators (eg tenecteplase as a single IV bolus). CI: •Previous intracranial haemorrhage. •Ischaemic stroke <6months. •Cerebral malignancy or AVM. •Recent major trauma/surgery/ head injury (<3wks). •GI bleeding (<1 month). •Known bleeding disorder. •Aortic dissection. •Non-compressible punctures <24h, eg liver biopsy, lumbar puncture. Relative CI: •TIA <6 months. •Anticoagulant therapy. •Pregnancy/<1wk post partum. •Refractory hypertension (>180/110). •Advanced liver disease. •Infective endocarditis. •Active peptic ulcer. •Prolonged/traumatic resuscitation
Without STEMI
- Monitor closely; record ECG while in pain
- If SaO2 <90% or breathless, low-flow O2
- Analgesia: Eg morphine 5–10mg IV + metoclopramide 10mg IV
- Nitrates: GTN spray or sublingual tablets as required
- Aspirin: 300mg PO. Consider need for second antiplatelet agent
- GRACE score
High risk:
• Rise in troponin OR:
• Dynamic ST or T–wave changes
• Secondary criteria—diabetes, CKD,
LVEF <40%, early angina post MI,
recent PCI, prior CABG, intermediate
to high-risk GRACE score
If yes:
1. Fondaparinux: 2.5mg OD SC or LMWH 1mg/kg/12h SC
2. Second antiplatelet agent (see text), eg
ticagrelor 180mg PO (or clopidogrel 300mg PO in lower risk, or prasugrel 60mg OD if proceeding to PCI)
3. IV nitrate if pain continues
(eg GTN 50mg in 50mL 0.9% saline at 2–10mL/h) titrate to pain, and maintain systolic BP >100mmHg
4. Oral b blocker
Prompt cardiologist review for angiography
1 Urgent (<120min after presentation) if ongoing
angina and evolving ST changes, signs of cardiogenic
shock or life-threatening arrhythmias
2 Early (<24h) if GRACE score >140 and high-risk patient
3 Within 72h if lower-risk patient
Conservative strategy (low-risk pt): • No recurrence of chest pain • No signs of heart failure • Normal ECG • —ve baseline (± repeat) troponin May be discharged (check troponin interval required with your laboratory and retest after delay if necessary). Arrange further outpatient investigation, eg stress test.
Grace score
Estimates admission-6 month mortality for patients with acute coronary syndrome.
PE
Initial:
Give high-concentration oxygen if oxygen saturations are <90%, targeting an initial oxygen saturation of 94% to 98%
Get an urgent senior review if systolic blood pressure (SBP) is <90 mmHg and the jugular venous pressure (JVP) is elevated to determine whether intravenous fluids need to be given. Give intravenous fluids if SBP is <90 mmHg and the JVP is not elevated
PE confirmed and h/d unstable:
- UFH IV, stop within 24 and convert to DOAC
- Thrombolysis (alteplase 10mg bolus IV then 90mg infusion over 2hrs) unless CI
(Absolute CI to both thrombolysis and anticoagulation, bleep senior advice and consider NA)
PE confirmed/suspected/Wells >4 and h/d stable:
- Anticoagulation and risk assess after DOAC adminstration (LMWH if unavailable) (apix 10mg BD, riva 15mg BD)
Thrombolysis CIs
Absolute contraindications:
Haemorrhagic stroke or stroke of unknown origin at any time
Ischaemic stroke in the preceding 6 months
Central nervous system damage or neoplasms
Recent major trauma/surgery/head injury (in the preceding 3 weeks)
Gastrointestinal bleeding within the last month
Known bleeding risk.
Relative contraindications:
Transient ischaemic attack in the preceding 6 months
Oral anticoagulant therapy
Pregnancy or within 1 week postnatally
Traumatic resuscitation (in relation to this episode of PE)
Refractory hypertension (systolic blood pressure >180 mmHg)
Advanced liver disease
Infective endocarditis
Active peptic ulcer.
Seek haematology advice if a patient with high-risk PE who is haemodynamically unstable has any contraindications to thrombolysis.
In practice, almost any contraindication to thrombolysis should be considered only relative in high-risk patients who present with haemodynamic instability.
This is because the mortality risk from high-risk PE is so high that it is likely to outweigh any bleeding risk from thrombolysis in this patient group
Shockable and Non-shockable rhythm management
Shockable: VF and Pulseless VT
1. Chest compressions 30:2, while applying self-adhesive defibrillation pads – one below the R clavicle and one at V6 position in MAL.
2. Administer shock, standing clear, less than 5 second break between chest compressions
3. Repeat chest compressions for 2 minutes and shock 4.Repeat again.
- After 3 shocks: Give adrenaline 1 mg IV and amiodarone
300 mg IV while performing a further 2 min CPR. (Withhold adrenaline if there are signs of ROSC)
- Repeat this 2 min CPR – rhythm/pulse check – defibrillation sequence with adrenaline after every other shock if VF/pVT persists.
Non-shockable: PEA and Asystole
1. Start CPR 30:2
2. Give adrenaline 1 mg IV as soon as intravascular access is achieved
3. Continue CPR 30:2 until the airway is secured – then continue chest compressions without pausing during ventilation
4. Recheck the rhythm after 2 min.
If a pulse and/or signs of life are present, start post resuscitation care
If no pulse/signs of life are present:
- Continue CPR
- Recheck the rhythm after 2 min
- Give further adrenaline 1 mg IV every 3–5 min (during alternate 2-min loops of CPR)
Both:
- Chest compressions 30:2
- Give adrenaline every 3-5 min
- Give amiodarone after 3 shocks
- Give oxygen, secure vascular access, get advanced airway in place
OD Paracetamol
PARACETAMOL
- minority of patients who present within 1 hour may benefit from activated charcoal to reduce absorption of the drug
- Acetylcysteine should be given if:
there is a staggered overdose or doubt over the time of paracetamol ingestion or
the plasma paracetamol concentration is on/above the treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours
- Infused over 1 hour (rather than 15 min) to reduce the number of adverse effects. (Acetylcysteine commonly causes an anaphylactoid reaction (non-IgE mediated mast cell release). If occurs, stop the infusion, and restart at a slower rate.)
King’s College Hospital criteria for liver transplantation
Arterial pH < 7.3, 24 hours after ingestion
or all of the following:
prothrombin time > 100 seconds
creatinine > 300 µmol/l
grade III or IV encephalopathy
Risk factors for paracetamol OD:
- patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s Wort)
- malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days
