Acute Care Flashcards
1
Q
What are the DDx of chest pain?
At least 15.
A
- Life treatening:
- CVS: ACS, pericarditis, cardiac tamponade, aortic dissection
- Repiratory: PE, pneumothorax (tension or spontaneous)
- GI: oesophageal rupture, pneumomediastinum
- Additional:
- Cardiac: stable angina
- respiratory: pneumonia
- GI: peptic ulcer disease, pancreatitis, cholecystitis, oesophagitis, reflux, oesophageal spasm
- MSK: rib fracture, costochondritis, zoster
- psychogenic/anxiety (diagnosis of exclusion)
2
Q
How do you assess a patient with chest pain?
A
- ABCs
- O2, IV cardiac monitoring, CXR, ECG
- Hx and physical exam
- Ix
- Bloods: FBC, UEC, glucose, Coags, CK-MB and troponin, D-dimer
- ECG
- CXR
- CT or V/Q, venous leg doppler to rule out PE in pts with intermediate to high probability
3
Q
What investigations would you order in your assessment in a patient with undifferentiated chest pain?
A
- blood work
- FBC, electrolytes, BUN/Cr, glucose
- CK-MB: if normal, does not rule out MI
- troponin I: more sensitive (but positive later than CK-MB; can have false positives in renal failure; must follow for 8 h post onset of symptoms)
- D-dimer: if negative, can rule out PE in low probability patients
- ECG
- always compare with previous
- PE and acute MI may have normal ECG in up to 50% of cases
- consider 15-lead ECG if hypotensive or if ECG shows inferior MI or AV node involvement
- CXR
- always compare with previous
- PE
- 50% completely normal
- atelectasis, elevated hemidiaphragm, pleural effusion
- aortic dissection
- change from previous CXR is the most accurate finding
- widened mediastinum (most consistent finding)
- CXR is normal in 20% of thoracic dissections
- pneumothorax
- may need inspiration and expiration views
- if large, may see tracheal shift (away from tension pneumothorax, towards a non-tension pneumothorax)
- V/Q scan or CT, venous leg Doppler, required to rule out PE in patients with intermediate or high probability - Well’s criteria
4
Q
Define what an acute coronary syndrome (ACS) is?
A
ACS uncludes unstable angina and evolving MI, which share a common underlyiing pathology - plaque rupture, thrombosis, and inflammation. However, ACS may rarely be due to emboli or coronary spasm in normal coronary arteries, or vasculitis. Usually divided into ACS with St-segment elevation or new onset LBBB - what most of us mean by acute MI; and ACS without ST-segment elevation - the ECG may show St depression, T wave inversion, non-specific changes, or be normal (including non-Q wave or subendocardial MI) The degree of irreversible myocyte death varies, and significant necrosis can occur without ST-elevation.
5
Q
What is the management of ACS?
A
- Pre-hospital - Ambulance
- Aspirin 300mg chewed (if no absolute CI) and GTN sublingual
- Analgesia: e.g. 5-10mg morphine IV + metroclopramide 10mg IV (not IM because of risk of cleeding with thrombolysis)
- In hospital
- O2, IV access, morphine (every 5 mins if needed), aspirin (if not already given)
- ST- elevation
- Primary angioplsty of thrombolysis, if no condraindication
- ß-blockers, e.g. atenolol 5mg IV unless contraindication, e.g. asthma
- ACE-inhibitor: consider starting ACE-i (e.g. (lisinpril 2.5 mg) in all normotensive patients within 24h of acute MI, especially if there is clinical evidence of heart fialure or echo evidence on LV dysfunction
- Consider clopidagrel 300mg loading following 75mg/day for 30 days
- ACS without ST segment elevation
- ß-blockers; e.g. atenolol 5 mg IV and nitrates IV unless contraindicated.
- Antithrombotic: fondaparinux if low bleeding risj and no angiography planned for 24h, otherwise consider low molecular weight heparin (e.g. enoxaparin 1mg/kg/12h SC for 2-8 days
- Assess risk - use GRACE score
- High risk (persistent or recurrent ischaemia, ST↓, DM, ↑troponin):
- GPIIb/IIIa antagonist (e.g. tirofiban), or bivalirudin and angiograpgy with 96h. Clopidagrel, in addition to aspirin, should be considered for up to 12 months
- Low risk (e.g. no further pain, flat or inverted T-waves, or normal ECG, and negative troponin:
- Clopidagrel if risk 1.5-3%/yr, discharge if a repeat troponin is negative. Treat medically and arrange further investigation if recurrent ischaemia.
- High risk (persistent or recurrent ischaemia, ST↓, DM, ↑troponin):
6
Q
What is the SOFA and qSOFA score?
MCQ question!
A
- Sepsis-related organ failure assessment score, also known as sequential organ failure assessment score (SOFA score), is used to track a person’s status during the stay in an intensive care unit (ICU) to determine the extent of a person’s organ function or rate of failure.
- The score is based on six different scores, one each for the respiratory, cardiovascular, hepatic, coagulation, renal and neurological systems.
7
Q
What are the parameters of the SOFA score?
MCQ question!
A
8
Q
What are the parameters for qSOFA?
MCQ question.
A
9
Q
What is the diagnostic criteria for HAP/VAP (ventilator acquired pneumonia)?
MCQ question.
A
- New pulmonary infiltrates (must be shown on CXR)]
- O2 requiremnt → worsening parenchymal function
- Purulent cough
- Fever
NOTE: 48 hours is not a diagnostic criteria but is assumed to be able to call the pneumonia HAP or VAP, otherwise it is CAP.
10
Q
What are the DDx for abdo pain in the emergency department?
A
- Life threatening:
- CVS: MI, aortic dissection (tearing pain), ruptured AAA
- GI: perforated viscus, hepatic/splenic injury, ischemic bowel (diffuse pain), strangulated hernia
- Gynecologic: ectopic pregnancy
- Additional Differential Diagnosis
- GI: appendicitis, diverticulitis, bowel obstruction, hepatitis, cholecystitis, pancreatitis
- Urinary: pyelonephritis, ureteral calculi, cystitis
- Genital
- female: tubo-ovarian abscess, ovarian torsion, ovarian cyst, salpingitis, PID, endometriosis
- male: testicular torsion, epididymitis, prostatitis
- Other: DKA, herpes zoster virus, intra-abdominal abscess, pneumonia, lead poisoning, porphyria, sickle cell crisis, acute angle closure glaucoma, Addison’s crisis, psychiatric
11
Q
What needs to be done on Hx and exam for abdominal pain in the ED?
A
- Hx:
- pain: SOCRATES
- broad differential, including GU, gynecological, GI, respiratory, and CV systems
- recent/remote abdominal trauma/surgeries
- most recent colonoscopy
- O/E:
- vitals, abdominal (including DRE, CVA tenderness), pelvic/genital, respiratory, and CVS asindicated by history
12
Q
What Ix need to be done on a patient with abdo pain in the ED?
A
- do not delay consultation if patient unstable
- CBC, electrolytes, glucose, BUN/Cr, U/A ± LFTs, lipase, β-hCG, ECG, troponins
- AXR (supine and upright): look for calcifications, free air, gas pattern, air fluid levels
- CXR upright: look for pneumoperitoneum (free air under diaphragm)
- U/S: biliary tract, ectopic pregnancy, AAA, free fluid
- CT: trauma, AAA, pancreatitis, nephro/urolithiasis, appendicitis, and diverticulitis
13
Q
What is the management of a patient with abdo pain in the ED?
A
- NBM, IV, NG tube, analgesics, consider antibiotics and anti-emetics
- growing evidence that small amoun ts of opioid analgesics improve diagnostic accuracy of physical exam of surgical abdomen
- consult as necessary: general surgery, vascular surgery, gynecology, etc.
14
Q
What are the differential diagnosis for dyspnea?
A
- Acute (minutes-hours)
- CVS: Ischemic heart disease, CHF exacerbation, cardiac tamponade
- Pulm:
- Upper airway obstruction (anaphylaxis, foreign body)
- Airway disease (asthma, COPD exacerbation, bronchitis)
- Parenchymal lung disease (ARDS, pneumonia)
- Pulmonary vascular disease (PE, vasculitis)
- Pleural disease (pneumothorax, tension pneumothorax)
- Respiratory control (metabolic acidosis, ASA toxicity)
- Psych: anxiety/psychosomatic
- Chronic (weeks-months)
- CVS: Valvular heart disease, decreased CO
- Pulm:
- Parenchymal lung disease (interstitial disease)
- Pulmonary vascular disease (pulmonary HTN, vasculitis)
- Pleural disease (effusion)
- Airway disease – asthma, COPD
- Metabolic: severe anaemia, hyperthyroidism
- Neuromuscular and chest wall disorders:
- Deconditioning, obesity, pregnancy, neuromuscular disease
15
Q
What are the life threatening causes of SOB in the ED?
A
- Resp:
- PE
- Pneumothorax
- anaphylaxis/asthma
- CVS:
- MI, aortic dissection
16
Q
What information do you need to get from Hx and exam about acute SOB?
A
- acute SOB is often due to a relatively limited number of conditions; associated symptoms and signs are key to the appropriate diagnosis
- substernal chest pain with cardiac ischemia
- fever, cough, and sputum with respiratory infections
- urticaria with anaphylaxis
- wheezing with acute bronchospasm
- chest tightness may be indicative of bronchospasm
- a sensation of rapid, shallow breathing may correspond to interstitial disease
- a sense of heavy breathing is typical of deconditioning
- ask about environmental or occupational exposures
- dyspnea may be the sole complaint and the physical exam may reveal few abnormalities (e.g. PE, pneumothorax)
- vitals including pulse oximetry
- wheeze (airway) vs. crackles (parenchymal), JVP, and murmurs
17
Q
What Ix need to be ordered on a pt with SOB in ED?
A
- blood work
- FBC and differential (hematocrit to exclude anemia), electrolytes, consider ABG/VBG
- serial cardiac enzymes and ECG if considering cardiac source
- imaging
- CXR (hyperinflation and bullous disease suggestive of obstructive lung disease, or changes in interstitial markings consistent with inflammation, infection, or interstitial fluid)
- CT chest usually is not indicated in the initial evaluation of patients with dyspnea, but can be valuable in patients with interstitial lung disease, occult emphysema, or chronic thromboembolic disease (i.e. PE)
18
Q
What information from Hx and exam would indicate a patient has an upper airway obstruction?
A
- History
- Stridor = sound on inspiration associated with airway narrowing
- stridor @ rest implies a reduction in airway diameter of >50%
- progression of symptoms
- positional exacerbation
- whether patient wakes @ night having difficulty breathing
- dysphagia
- drooling
- severe obstruction -> coughing becomes difficult -> chest infections
- Examination
- Airway assessment
- Neck examination
- Nasal endoscopy – photos helpful, doesn’t involve LA to cords which could precipitate total airway obstruction, beaware that a nice view in the sitting position doesn’t mean the same in the supine position.
19
Q
What are the possible causes of coma?
HINT: AEIOU TIPS
A
- Acidosis/Alcohol
- Epilepsy
- Infection
- Oxygen (hypoxia)/Opiates
- Uremia
- Temperature/Trauma (especially head)
- Insulin (too little or too much)
- Psychogenic/Poisoning
- Stroke
20
Q
The majority of comas are due to toxic/metabolic causes. What are the DDx?
HINT: METABOLIC
A
M – Major organ failure
E – Electrolyte/Endocrine
T – Toxins/Temperature
A – Acid disorders
B – Base disorders
O – decreased Oxygen level
L – Lactate
I – Insulin/Infection (sepsis)
C – Cardiac/hyperCalcemia
21
Q
What information needs to be gathered from Hx and Exam of a patient with altered conscious state?
A
- History
- obtain collateral from family, friends, police, paramedics, old chart, etc.
- onset and progression
- abrupt onset suggests CNS hemorrhage/ischemia or cardiac cause
- progression over hours to days suggests progressive CNS lesion or toxic/metabolic cause
- preceding events
- it is essential to determine patient’s baseline LOC
- antecedent trauma, seizure activity, fever
- past medical history (e.g. similar episode, depression, overdose)
- Physical Exam
- ABCs, vitals including temperature, cardiac, chest, respiratory, abdominal exam
- complete neuro exam, in particular examination of the eyes (pupil size and reactivity), look forMedicAlert® bracelet
22
Q
What Ix need to be ordered in a patient with altered consciousness?
A
- blood work
- rapid blood sugar, FBC, UECs, BUN, LFTs, glucose, serum osmolality, VBG, PT/PTT/INR, troponins
- serum EtOH, acetaminophen, and salicylate levels
- imaging
- CXR, CT head
- other tests
- ECG, U/A, UTox
23
Q
How do you manage a patient with altered consciousness in the ED?
A
- administer appropriate universal antidotes
- thiamine 100 mg IV if history of EtOH or patient looks malnourished
- one ampule D50W IV if low blood sugar on finger-prick
- naloxone 0.4-2 mg IV or IM if opiate overdose suspected
- distinguish between structural and toxic-metabolic coma
- structural coma
- pupils, extraocular movements, and motor findings, if present, are usually asymmetric
- look for focal or lateralizing abnormalities
- toxic-metabolic coma
- dysfunction at lower levels of the brainstem (e.g. caloric unresponsiveness)
- respiratory depression in association with an intact upper brainstem (e.g. equal and reactive pupils)
- extraocular movements and motor findings are symmetric or absent
- structural coma
- essential to re-examine frequently because status can change rapidly
- diagnosis may become apparent only with the passage of time
- delayed deficit after head trauma suggestive of epidural haematoma (characteristic “lucid interval”)
24
Q
Definition of seizures.
A
- continuous seizure activity for 5 minutes or more without return of consciousness, or
- recurrent seizures (2 or more) without an intervening period of neurological recovery
25
What are the goals of management in status epilepticus?
1. Resuscitation to prevent secondary brain injury and maintain cerebral perfusion pressure
2. Terminate seizure
3. Decrease cerebral metabolic rate
4. Diagnose and treat cause
5. Treat complications
26
How is a patient in status epilepticus resuscitated?
* Attend to ABCS and address life threats
* Manage airway with recovery position, airway adjuncts and intubation if required
* Optimise oxygenation and provide ventilatory support as needed (prone to hypercapnia)
* Early IV or IO access, optimise cerebral perfusion pressure
* Treat hypoglycaemia and life-threatening electrolyte disturbance if present
* Maintain normothermia
* Give relevant antidote if due to toxic agent (e.g. pyridoxine for isoniazid)
27
HOw is status epilepticus terminated?
* First line therapiesBolus dose benzodiazepines
* Midazolam 0.1mg/kg IV – also buccal or IM (IM not inferior to IV lorazepam)
* Lorazepam 0.1mg/kg IV (onset in 3-5 minutes and last hours; preferred for longer acting effects)
* Diazepam 5mg IV/PR (avoid IM as painful) (onset in ~1 minute but lasts only about ~20 min for antiseizure activity)
* Clonazepam
* Second line therapies (typically requires intubation and mechanical ventilation)
* Phenytoin 15-20 mg/kg IV over 30 minutes or longer
* should be used to terminate seizures as a sole agent, always with benzodiazepines
* some regard phenytoin as a first line therapy, however not all seizures require therapy in addition to termination with benzodiazepines
* avoid if usually on phenytoin
* avoid rapid push to risk of cardiovascular toxicity from the propylene glycol diluent
* fosphenytoin is not available in Australia
* Valproic acid — 40 mg/kg IV over 10 min (may give additional 20 mg/kg over 5 min if still seizing)
* Leviteracetam (off label use for status epilepticus)
* Third line therapies (for refractory status epilepticus; typically require intubation and ventilation and cEEG monitoring)
* propofol 2-3mg/kg IV then \<4mg/kg/hr
* midazolam IV infusion
* Barbiturates
* Phenobarbitone infusion 10mg/kg IV boluses -\> 0.2-0.4mg/kg/min
* Thiopentone 4mg/kg IV (then repeat boluses or infusion targetting burst suppression)
* Clonzepam IV infusion
* Fourth line therapies
* Thiopentone (if not already started)
* Volatile anaesthetic agent (e.g. isoflurane)
* Ketamine infusion
* Magnesium
* Lignocaine
28
What is the recovery position?
Lateral recumbent
29
Define shock.
Inadequate organ and tissue perfusion with oxygenated blood
30
How is shock classified? and give examples of each
* Hypovolaemic:
* Haemorrhage
* Severe burns
* high output fistulas
* Dehydrations (diarrhoea, DKA)
* Cardiogenic
* Myocardial ischaemia
* Dysrhythmias
* CHF
* Cardiomyopathies
* cardiac valve problems
* Distributive (vasodilation)
* Septic
* Anaphylatic
* Neurogenic (spinal cord injury)
* Obstructive
* Cardiac tamponade
* Tension pneumothorax
* PE
* Aortic stenosis
* Constrictive pericarditis
31
What are the clinical features of shock?
* early: tachypnea, tachycardia, narrow pulse pressure, reduced capillary refill, cool extremities, and reduced central venous pressure
* late: hypotension and altered mental status, reduced urine output
32
What is a vasopressor?
An agent that causes vasoconstriction and increases mean arterial pressure
33
What is an ionotrope?
An agent that alters the force or energy of muscle contraction (increases cardiac contractility).
34
What methods can be used to treat an anterior dislocation of the should?
1. Leverage techniques:
1. _Kockers method_: involves traction to the elbow with external rotation of the humerus and adducting the elbow toward the chest. This method can be associated with neurovascular complications and proximal humerus fractures.
2. _Milch technique_: involves traction to the elbow with external rotation of the humerus and adducting the elbow toward the chest. This method can be associated with neurovascular complications and proximal humerus fractures.
2. Traction methods:
1. _Hippocratic method_: place heel into patient’s axilla and apply traction to arm
2. _Stimson's method:_ while patient lies prone with arm hanging
over table edge, hang a 5 lb weight on wrist for 15-20 min
3. _Matsens traction couteraction_: assistant stabilizes torso with a folded sheet wrapped across the chest while the surgeon applies gentle steady traction
3. Scapular manipulation
35
What are the common features of organophosphate posioning?
* anxiety
* restlessness
* dizziness
* headache
* nausea
* hypersalivation
* vomiting
* abdominal colic
* diarrhoea
* bradycardia
* sweating
* Muscle weakness and fasciculation may develop and progress to generalised flaccid paralysis.
36
Describe the pathogenesis of organophosphate poisoning?
Organophosphorous insecticides are all absorbed through the bronchi and intact skin, as well as through the gut, and inhibit cholinesterase activity, thereby prolonging and intensifying the effects of acetylcholine.
37
What is the Rx of organophosphate poisoning and how does it work?
* Atropine will reverse the muscarinic effects of acetylcholine and is given in a dose of 2 mg as atropine sulphate every five to 10 minutes, until the skin becomes flushed and dry, the pupils dilate, and tachycardia develops.
* Pralidoxime mesylate (P2S), a cholinesterase reactivator is used as an adjunct to atropine, in moderate or severe poisoning, but it is only effective if given within 24 hours. It produces muscle improvement within 30 minutes but further doses may be required.
38
What is the emergency management of anaphylaxis?
* Immediate initial management (call for help and perform concurrently)
* give 0.5 mL of 1:1,000 epinephrine IM to lateral thigh (0.01 mL/kg up to 0.4 mL for children)
* remove causative agent if possible
* if severely compromised ABC or LOC, consult ICU immediately
* otherwise, provide 100% O2 through mask, give bolus 1,000 mL (20 mL/kg for children) crystalloid IV, then reassess; if IV access difficult, give fluid through intraosseous route
* have continuous pulse oximetry and telemetry monitoring
* frequently monitor BP
* secondary treatment
* diphenhydramine (Benadryl®) 50 mg IM or IV q4-6h
* methylprednisolone 50-100 mg IV (dose depending on severity)
* salbutamol (Ventolin®) via nebulizer if bronchospasm
39
What is the clinical presentation of anaphylaxis?
* classic presentation of anaphylaxis includes
* rapid onset and progression of symptoms
* life-threatening compromise of one or more of airway (breathing/swallowing difficulty, stridor, voice change), breathing (SOB, hypoxemia, wheezing, respiratory arrest), and circulation (tachycardia, hypotension, confusion, decreased urine output, chest pain)
* involvement of skin (erythema, urticaria, warmness) and/or mucosa (angioedema, obstruction, GI symptoms) not always present
* the presentation of anaphylaxis is diverse and there is no one specific symptom or sign for it
* combinations of symptoms and signs will make anaphylaxis more likely
* life-threatening differentials for anaphylaxis include asthma and septic shock
40
After the emergent management of anaphylaxis what needs to be done for the patient?
* monitor for 4-6 h in ED (minimum) and arrange follow-up with family physician in 24-48 h
* can have second phase (biphasic) reaction up to 48 h later, patient may need to be supervised (oral steroids on discharge may prevent this)
* educate patient on avoidance of allergens
* 3-day course of:
* H1 antagonist (cetirizine 10 mg PO OD or Benadryl® 50 mg PO q4-6h)
* H2 antagonist (ranitidine 150 mg PO OD)
* corticosteroid (prednisone 50 mg PO OD) generally given for 5 d
41
What are the ECG features that contribute to the diagnosis of hyperacute anterolateral MI?
* ST segments in anterior and lateral leads (aVL, I, and V2-6) and/or T wave inversion
* Increased T wave amplitude and narrow
42
WHat are prolonged QT interval associated with?
* Congenital abnormalities like Romano-Ward syndrome
* Hypocalcaemia, and
* Drugs (such as amiodarone).
43
