Introduction

Acute Coronary Syndromes is an umbrella term for a spectrum of disease caused by ischaemia (and in some cases infarction) of myocardium (loss of blood supply to heart muscle). It is a medical emergency and required immediate hospital admission.

  • STEMI – ST elevation MI
    • Diagnosable on the basis of classical ECG changes
  • NSTEMI – non-ST elevation MI
    • Usually diagnosed on the basis of a suggestive history, with positive biochemical markers – e.g. positive troponin
  • Unstable angina – ischaemia, without infarction
    • No obviously evident ECG changes (there may be some transient changes), negative troponin, often a history suggestive of ACS. Unstable angina is significant due to the high risk (50%) of MI in the subsequent 30 days. Not to be confused with stable angina
They are grouped together because – they all have a common mechanism – rupture or erosion of the fibrous cap of a coronary artery plaque.
Imagine it like a spectrum – with unstable angina at the less severe of the scale end, and STEMI at the other – NSTEMI is in the middle.
A textbook presentation is an acute onset central or left sided chest pain, which often comes at rest, in the morning, gradually increasing in intensity over a period of minutes, with radiates down the left arm, associated with diaphoresis (sweating), and pre-syncopal or syncopal symptoms. However, about 30% of patients present without pain.
Those with STEMI may be diagnosed outside of hospital on the basis of their ECG (e.g. by ambulance or in primary care) and bypass the emergency department taken straight to the catheter lab for PCI (angioplasty). However, most patients will be assessed in the emergency department. The mainstay of diagnosis is a combination of history, ECG and biochemical markers (usually troponin). Diagnosing STEMI is straightforward – based on the ECG. NSTEMI is diagnosed on the basis of a positive troponin. The main diagnostic challenge in practice is deciding who is a risk of unstable angina, and who is safe to be discharged home. There are various diagnostic tools to assist with the process, such as the HEART score.
  • STEMI, NSTEMI and unstable angina can all have a similar clinical presentation
  • Pathologically STEMI is often associated with complete or almost complete occlusion of one or more of the coronary arteries, whereas NSTEMI and unstable angina are associated with partial occlusions
For more information on the pathology, and a general overview of atherosclerotic disease, see the Atherosclerosis article

 

Epidemiology

  • Coronary heart disease is the most common cause of death in the UK
  • In the case of MI:
    • 50% of deaths occur within 2 hours of onset of symptoms
    • 15% of cases of MI are fatal
  • Incidence of 300 000 cases per year
  • CAD (coronary artery disease) accounts for about 3% of admission to UK hospitals each year

Aetiology

Non-modifiable

  • Age
  • Gender (male)
  • FH of IHD – only significant if symptoms presented before the age of 55 in the relative

Modifiable

Controversial

  • Stress
  • Type ‘A’ personality
  • LVH – left ventricular hypertrophy
  • Cocaine use
    • Acutely can cause coronary vasospasm which can cause MI
    • Chronically increases the risk of MI from a traditional atherosclerotic disease process
  •  ↑ fibrinogen

Symptoms

  • Chest pain! Can radiate down the inside of the arm, and into the neck and jaw and can last up to a couple of hours. May also radiate to the epigastrium or back
    • More predictive for MI if it radiates to both arms or the right arm (contrary to the classical textbook definition of radiating down the left arm!)
    • Typically a “crescendo pain” with increasing severity over a period of several minutes after onset
    • Typically a “mid range” pain – e.g. 5-7 out of 10
  • Sweating – in this circumstance is often referred to as diaphoresis
  • Breathlessness – indeed in many cases this may be the only symptom
  • Syncope – fainting – if this occurs, then it will be a result of severe arrhythmia, or severe hypotension.
  • Tachycardia
  • Vomiting and sinus bradycardia– this may occur as a result of excessive vagal stimulation, which is most common in inferior MI
    • Be aware that nausea and vomiting may also be aggravated by opiates given for pain relief
  • Distress, also sometimes a ‘feeling of impending doom’
  • Sudden death – this usually occurs from ventricular fibrillation or asystole. Most of these deaths occur within the first hour.
    • If the patient survives the first hour, then the likelihood of serious arrhythmias remains, but diminishes with each subsequent hour. So, it is important for patients to get help as soon as possible!
    • Cardiac failure is the major cause of death in those that survive the first few hours. Whether or not cardiac failure develops is dependent on the extent of myocardial damage.
  • Remember, infarction can occur in the absence of any physical signs
  • MI (and stroke) is often more common in the morning. This is thought to be because BP lowers during the night, and then rises again when the person wakes up. This higher BP may then dislodge any thrombus that has formed overnight.

Factors that are more specific

Some factors are particularly significant for the likelihood of ACS compared to other causes of chest pain. These include:

  • Pain >15 minutes
  • Pain that radiates to the arms or jaw
  • Diaphoresis
  • Vomiting
  • Exertional chest pain

Features that suggest non-ACS chest pain include:

  • Reproducible chest pain (i.e. tender chest wall or positional pain)
  • Pleuritic chest pain

Features that are not useful to predict the likelihood of ACS

  • Severity of pain
  • Response to GTN
  • Response to ant-acids / PPIs

The Atypical Presentation

  • MI without chest pain – sometimes referred to as a silent MI
  • Atypical presentation is particularly important in MI – because it is not very atypical
  • 30% of case of MI present without chest pain. This is particularly important in:
    • Women
    • Those with diabetes
    • The elderly
  • In the above populations, particularly significant historical features include:
    • Shortness of breath – especially if on exertion (“SOBOE”)
    • Generalised weakness
    • Dizziness
  • Other symptoms associated with a silent MI include:

Signs

Signs of impaired myocardial function

  • 3rd / 4th heart sounds
  • Pan systolic murmur
  • Pericardial rub
  • Pulmonary oedema – crepitations in the lungs
  • Hypotension
  • Quiet first heart sound
  • Narrow pulse pressure (difference of <40mmHg)
  • Raised JVP

Signs of sympathetic activation

  • Pallor (basically looking pasty. It can be generalised or localised, but is only really clinically significant if generalised. Most evident in the palms and on the face)
  • Sweating
  • Tachycardia

Differentials

Cardiac

  • Angina
  • Pericarditis
  • Myocarditis
  • Aortic dissection

Pulmonary

Oesophageal

  • Oesophageal reflux
  • Oesophageal spasm
  • Tumour
  • Oesophagitis

Pathology

MI is almost always due to occlusive thrombus formation at the site of rupture or erosion of an atheromatous plaque. The pain experienced is usually the same as angina, but lasts longer and may be more severe.
  • Patients should call an ambulance if they experience ‘angina type pain’, which, after using GTN spray does not subside within 15 minutes.
  • The pain is often excruciating – look at the patients face / expression / pallor to determine the seriousness of the pain
There are two different mechanisms. Either:
  • the fibrous cap of the plaque itself gets a superficial injury, and a thrombus forms on it, or,
  • in more advanced, unstable plaques, the fibrous cap completely ruptures, and not only can some of the contents escape, but blood can also enter the plaques, forming a thrombus within the remaining cap of the plaque.
Platelets then release serotonin and thromboxane A2 and this causes vasoconstriction in the area resulting in reduced blood flow to the myocardium, and ischaemic injury.
 

Differentiating types of MI

  • Transmural MI – this is an infarct that causes necrosis of tissue through the full thickness of the myocardium
  • Nontransmural – this is an MI that does not cause necrosis through the full thickness of the myocardium

Diagnosis and Investigations

ECG changes

Early – within hours

  • Peaked T wave (very tall T wave)
  • Raised ST-segment

Within 24h

  • Inverted T waves – this may or may not persist
  • ST segment returns to normal. Raised ST segments may persist if a left ventricular aneurysm develops

Within days

  • Pathological Q waves form – these may resolve in 10% of cases
    • We say the Q wave is pathological if it is >25% of the height of the R wave, and/or it is greater than 0.04s width (1 small squares) and/or greater than 2mm height (2 small squares)
    • Q waves are also a sign of a previous MI – the changes in Q waves are generally permanent. The changes in T waves may or may not revert. The ST segment can return to normal within hours.
    • Non-q-wave infarcts are infarcts that occur without the changes seen in the Q waves, but still with the ST and T changes.
Typical picture of changes
ST elevation – then later, T inversion – , then later, Q wave appears
Other patterns of ECG change:
  • ST-depression
  • Reciprocal change – sometimes seen in STEMI. This refers to a phenomenon whereby there is ST DEPRESSION in some leads, in the presence of ST elevation in others. This occurs as the ECG leads are viewing the heart from different angles. the ST depression will typically occur in leads viewing the heart at the opposite angle to those showing ST elevation. The presence of reciprocal change is thought to indicate an earlier presentation of MI but is not particularly associated with different outcomes.
REMEMBER!
  • ST depression – Ischaemia – the damage is reversible (with the right treatment)
  • ST elevation – Infarction – damage is irreversible
STEMINSTEMIUnstable angina
ECG
  • ST elevation

OR

  • New LBBB
May be normal, or may include:

  • Non-specific changes
  • T-wave inversion
  • Hyper-acute T waves
  • ST depression
Often normal, or may include:

  • Non-specific changes
  • T-wave inversion
  • Hyper-acute T waves
  • ST depression
Troponin
  • Elevated
  • Don’t wait for the result!
  • Raised serial troponin
  • Normal serial troponin

STEMI

  • Diagnosis is usually straight forward on the basis of the ECG
  • ST elevation. Significant if:
    • ST elevation >1mm in 2 contiguous (consecutive) leads except V2 or V3
    • ST elevation >2mm in V2 or V3 in men >45
    • ST elevation >2.5mm in V2 or V3 in men <45
    • ST elevation >1.5mm in V2 or V3 in women of any age
ST elevation ECG

An elevated ST segment

ECG showing Inferior STEMI

ECG showing Inferior STEMI. Note the marked ST elevation in leads II, III and aVF, and the ST depression on V2, V3 and V6 (often termed ‘reciprocal change’ when it is associated with ST elevation in other leads). Also note that there is not (yet) any T wave inversion in this patient.

  • New onset Left Bundle Branch Block (LBBB) is considered equivalent to ST elevation
    • For any patient with new onset chest pain and LBBB on ECG you need to compare to an old ECG to see if the LBBB is new. If none is available, consider STEMI until proven otherwise.
    • Scarbosa criteria are used to assess patients with previously known LBBB for ST elevation – as it can be difficult to discern ST elevation in the presence of LBBB. If any of the following are preens,t then Scarbos’a criteria are met:
      • Concordant (going in same direction as QRS spike) ST elevation >1mm in any lead
      • ST depression >1mm in V1, V2 or V3
      • Discordant (going in opposite direction to QRS) ST elevation of >5mm in any lead
Left Bundle Branch Block

An example of Left Bundle Branch Block – without any signs that would fulfil the Scarbosa Criteria. Note the typical features of LBBB including widened QRS (>120ms), “negative” QRS complex in lead V1 (more properly called an “rS” complex) and “positive” QRS complex in lead V6 (“R”). For more help with ECGs, see Understanding ECGs

  • The location of the ST changes can indicate the location of the MI
Location of MI based on ECG

Location of MI based on ECG

NSTEMI

NSTEMI is usually diagnosed on the basis of:

  • A suggestive history
  • Elevated troponin levels
    • Be aware that any condition that causes myocardial damage can result in an elevated troponin. Examples of other causes of elevated troponin include PE, myocarditis, renal failure (chronically raised).
    • What is particularly important is the pattern of the troponin result (see below)
  • ECG changes
    • An absence of ST evevation
    • ECG may be normal
    • There may be other changes on ECG to suggest MI. These might include:
      • ST depression
      • Hyperacute T wave (tall pointy T waves) – often an early sign which resolve but the time the patient is seen in hospital
      • TWI (T-wave inversion) – a late sign, often indicates previous MI
      • Non-specific ST changes

Unstable angina

Unstable angina is distinguishable from NSTEMI only through troponin results.

  • Troponin – negative
  • ECG changes – as for NSTEMI above

Troponin Testing

Troponin testing is changing. Your local hospital may be using traditional troponin testing, or the newer high sensitivity troponin. Two types of troponin can be tests for – troponin I and troponin T. The exact troponin tested is not significant, but there are important difference between traditional and high sensitivity tests.

  • Traditional troponin is a positive or negative test. Serial troponin tests are performed over several hours (typically over 6-8 hours), and any detected troponin results in a “positive” test, and therefor a diagnosis of NSTEMI.
    • Troponin levels rise from 2-24 hours after onset of pain, and peak at around 24 – 48 hours, and return to baseline in 5-14 days
  • High sensitivity troponin testing is a little more subtle
    • 50% of the healthy population have an undetectable troponin
    • 50% of the healthy population have a detectable level of troponin
    • The exact reference range will very from centre to centre. At my hospital, the “normal range” is quoted as <16ng/L
    • The recommended test method is TWO troponin tests, 2 hours apart, within 3 hours of the onset of chest pain
      • single negative troponin test is acceptable as a ‘rule out’ (for ACS) if it is >3 hours since the onset of pain
    • positive test is defined as an increase in troponin between the two tests. The exact level of increase which signifies NSTEMI is hotly debated, but a 20% increase is a roughly agreed upon figure
      • Take this with a pinch of salt – a result of 4ng/L and then 5ng/L is not significant, but a result of 50ng/L and then 60ng/L may be
      • Often in practice interpretation is quite straight forward – e.g. the initial result may be negative, and a subsequent result may be in the hundreds or even thousands
    • Bear in mind other causes of raised troponin. These are less likely to show a significant increase between the two tests, although they may mimic STEMI. Causes include:
      • Renal failure
      • Myocarditis
      • PE
      • Pericarditis
      • Heart failure
      • Arrhythmia
  • The troponin level is correlated to risk of death from ACS
    • Negative troponin result is strongly predictive of good 30-day prognosis
  • Creatine kinase (CK)
    • Found in skeletal and myocardial muscle
    • Raised after any sort of muscle trauma, also raised after MI
    • Previously used in MI diagnosis, has now been superseded by troponin testing in almost all centres

CXR

Don’t delay treatment whilst waiting for the CXR! Changes may include:

  • Cardiomegaly
  • Pulmonary oedema and other signs of treat failure
  • Widened mediastinum

Other Blood Tests

Glucose – not only does this help you treat any diabetes present, but evidence suggests that patients with a high glucose on admission have a worse prognosis- thus you should treat these patients more aggressively.
Lipids – checking for raised cholesterol – although this isn’t strictly necessary as all MI patients are given a potent statin (e.g. atorvastatin) for secondary prevention regardless of the cholesterol level.
FBC – get a provisional platelet level before anticoagulation. Check for anaemia.

Acute Management

Pre-hospital
  • Call ambulance
  • Aspirin 300mg orally – unless an obvious contraindication
  • Pain relief, e.g. 5-10mg morphine + metoclopramide (anti-emetic)10mg IV – avoid IM injections as there is a risk of bleeding – and you just gave loads of aspirin!
  • Sublingual GTN (unless hypotensive)
    • Comes as a sublingual spray or sublingual tablet
    • Typical dose might be 300-600mcg PRN
    • Give until symptom relief is achieved (chest pain / SOB resolves)
    • There is no “maximum” dose for GTN – providing the HR is >50, or the systolic BP >90
  • Oxygen – if sats are <94%
Hospital
  • ECG as soon as possible – it is also likely that this will have been done in the ambulance.
    • It is important to differentiate STEMI for other ACS / other causes of chest pain as soon as possible
    • Serial ECGs are a very important part of the emergency work-up of chest pain. Dynamic ECG changes refer to intermittent and changing ECG findings and are highly suggestive of ACS
  • Assess oxygen saturation – if sats are above 94% you do not need to give oxygen (in practice, people are often given oxygen regardless but this is not best practice). If sats are below 94% then give high-flow oxygen via a non-rebreather mask (i.e. with an inflated bag on)
  • In patients with known COPD, aim for sats between 88-92% – give oxygen via a 24% or 28% Venturi mask (colour coded) and get an ABG.

Get IV access – take bloods for

  • FBC, U+E, glucose, lipids, troponin, ABG

Take history / make brief assessment

  • History of CHD?
  • Risk factors?
  • Contra-indications to thrombolysis

Do a cardiac examination

  • Pulse
  • BP
  • JVP
  • Murmurs
  • Signs of heart failure
  • Peripheral pulses
  • Signs of previous surgery
  • ECG

Give 300mg aspirin if not already administered
Give 5-10mg morphine and metoclopramide 10mg IV if not already administered

Give GTN sublingually if not already given – BUT don’t give with systolic BP <90, or with a HR <50.

Definitive management

  • STEMI
    • Refer to cardiology urgently
    • If angioplasty (aka percutaneous coronary intervention – PCI) is available – activate the catheter lab – best outcomes are achieved in patients who make it to the cath lab within 120 minutes of onset of pain
    • PCI should be considered for all patients presenting within 12 hours of onset of pain – although proven benefit for those >120 minutes since onset of pain is debated
    • PCI can involve either balloon angioplasty or primary coronary artery stenting. Stenting seems to be associated with better outcomes – in particularly reduced risk of re-infarction. As such, it is recommended by NICE as the PCI intervention of choice
    • PCI is superior to thombolysis for long-term outcomes
      • Primary PCI – PCI given within the 120 minute window
      • Rescue PCI – PCI after failure of thrombolysis
      • Facilitated PCI – PCI deliberately planned in conjunction with thromboylsis – has no proven benefit over PCI alone and is such is not used in clinical practice
    • If angioplasty is not available – give THOMBOLYSIS – the sooner the better – The British Heart Foundation advises that it should be given no greater than 90 minutes after initial onset of chest pain, and ideally no greater than 60 minutes if possible
      • Streptokinase, recteplacse or tenecteplase are commonly used thrombolysis drugs
        • Streptokinase use results in development of antibodies and should only be given once in a lifetime
      • BUT – DONT GIVE THROMBOLYSIS TO THOSE WITHOUT ST ELEVATION!
      • Pre-hospital thrombolysis (i.e. via ambulance) is indicated if PCI is not available with 120 minutes of onset of pain
      • Most effective within the first hour, but an be given up to 12 hours after symptom onset
      • 1-2% risk of intracranial haemorrhage
      • Beware of contraindications – hx of bleeding disorder, recent bleeding event, recent trauma or surgery, recent cerebrovascular event.
    • Give heparin
      • e.g. unfractionated heparin infusion (follow local hospital guidelines), or low molecular weight heparin (e.g. enoxaparin – for 2-8 days)
    • Give a glycoprotein IIb/III inhibitor
      • These are usually given alongside PCI and reduce the risk of immediate vascular occlusion
      • They work by reducing platelet aggregation and thrombus formation
      • e.g. abciximab, eptifibatide, and tirofiban
  • NSTEMI
    • Refer to cardiology
    • PCI is also considered first line treatment for those with high risk NSTEMI
    • Thrombolysis is NOT INDICATED for NSTEMI
  • Unstable angina
    • If the history is convincing, but the investigations are normal, consider unstable angina
    • Consider a risk score – such as the HEART score to help you decide whether or not to discharge home, or refer to cardiology for admission
    • Patients should undergo ECG stress testing (‘treadmill test’)
  • For all confirmed ACS patients
  • Consider prasugrel, ticagrelor or clopidogrel – exact drug and dose often under advise from cardiology or in conjunction with local hospital policy
    • In conjunction with aspirin, long term use of clopidogrel is associated with better outcomes
  • Start a β-blockerusually atenolol 5mg IV. Do not give if asthma or right ventricular failure
    • β-blocker given within hours of onset of symptoms reduce mortality, and re-infarction risk
    • Usually IV dose on admission and the continued orally indefinitely
    • Long term beta-blocker use reduces the risk of mortality by 25%
    • β – blockers have antihypertensive effects, by encouraging peripheral vasodilation, and it also reduces cardiac output, by reducing the rate and contractility of the heart. They also reduces renin secretion.
  • ACE-inhibitors
    • Should be given to all confirmed ACS patients
    • Reduce mortality regardless of blood pressure
    • Titrate to the maximum tolerated dose over a period of weeks (monitor BP and symptoms of hypotension)
    • Reduces mortality by 25-30% at 2 years
  • Statin
    • Start as soon as possible for all ACS patients, regardless of cholesterol levels
    • Aim for total cholesterol <4mmol/L and HDL >1.0 mmol.L
  • Patients with diabetes, consider:
  • Consider DVT prophylaxis
  • Hospital admission with constant ECG monitoring
  • Examine daily – including heart lungs and legs – for complications
  • Cardiac enzymes – every day for 3 days – should see troponin levels begin to fall
  • DISCHARGE – if no complications, most patients are discharged after 5-7 days.
    • Work – patients should return to work after 2 months. Certain careers may no longer be allowed:
      • Airline pilot
      • Air-traffic controller
      • Driver – Some driving jobs allow patients to return to work if they meet certain criteria
      • Some physically demanding jobs (e.g. involving heavy lifting) may not be suitable

MONA Mnemonic for acute management of MI

All ACS patients

  • M – Morphine
  • O – Oxygen (if sats <94%)
  • N – Nitrates
  • A – Aspirin

If High Risk NSTEMI or STEMI – MONAC

  • M – Morphine
  • O – Oxygen
  • N – Nitrates
  • A – Aspirin
  • C – Clopidogrel

After acute event when stable

  • Beta-blocker
  • Ace-Inhibitor
  • Statin

Long term management

Long term management measures are also often referred to as Secondary Prevention
  • i.e. reducing the risk of a ‘secondary’ event
Cardiac rehabilitation programs
All patients should be offered a place on a cardiac rehabilitation program, and programs should always involve an exercise component. You should not exclude a patient from any part of the program if they chose not to attend any individual parts
These programs generally offer support to achieve the goals listed below:

Smoking cessation
Increase in exercise – encourage regular daily exercise, and at least 30 minutes, 3x/week strenuous exercise

  • Sex – Should avoid for 1 month after MI
  • Travel – avoid air travel for 2 months

Reduction in weight
Reduction in alcohol intake
Dietary modification (reduced fat intake) – diet should be:

  • High in – oily fish, fibre, fresh fruit and veg
  • Low in – saturated fat

Review

  • At 5 weeks – for complications, and angina. Treat angina in normal method. Consider angioplasty if severe
  • At 3 months – check for raised cholesterol and consider statin if not already prescribed.

COBRA-A mnemonic for Secondary Prevention in ACS

  • C – Clopidogrel – antiplatelets
  • O – Omacar – Omega 3
  • B – Bisoprolol – β-blocker
  • R – Ramipril – ACE-i
  • A – Aspirin
  • A – Atorvastatin – very potent statin!
For information on the mechanisms and side-effects of these drugs, please see the Cardiovascular Drugs Article

Complications of MI

  • Cardiac arrest
  • Bradycardia, heart block
  • Tachyarrhythmias
  • Left ventricular failure
  • Right ventricular failure
  • Pericarditis
  • DVT & PE
  • Systemic embolus
  • Cardiac tamponade
  • Mitral Regurg
  • Ventricular septal defect
  • Late malignant ventricular arrhythmias
  • Dressler’s syndrome
  • Left ventricular aneurysm
  • Mural thrombus – this is a thrombus attached to the wall of the endocardium in a damaged area, or sometimes it is attached to the aortic wall over an intimal lesion. MI leads to akinetic areas of ventricular wall. This stasis allows the formation of a thrombus on the wall. The larger the infarct, the greater the risk of thrombus. Parts of the thrombus can easily break off an embolise. Common sites of ischaemia are; brain, spleen, gut, kidney, lower limbs.
  • Ventricular wall rupture – this occurs about 5-10 days after the initial infarct. At this time the myocardium is particularly soft. Blood can then come out of the rupture, and enter the pericardial sack, causing haemopericardium. This usually leads to cardiac tamponade as it is an acute effect. This classically presents with electromechanical dissociation – a perfectly normal ECG, but no cardiac output and no pulse. As you know – PEA (pulseless electrical activity) is a non-shockable rhythm – and thus almost always results in death
  • Ventricular aneurysm – this is a late complication of a transmural MI. the infracted muscle will be replaced by a thin layer of collagenous scar tissue, that will gradually stretch as intraventricular pressure rises during systole. The aneurysm itself has complications of left ventricular failure, arrhythmias, mural thrombus. Rupture of the aneurysm is rare.
  • Mitral valve incompetence – commonly caused by ischaemic damage to the papillary muscles, especially in posterior infarcts. Post ischaemic fibrosing and shortening of the papillary muscles can also cause incompetence. In some patients, the papillary muscles can be completely destroyed by the infarct, resulting in instant and complete torrential mitral valve incompetence.

Dressler’s syndrome

An autoimmune pericarditis, provoked by MI. Occurs in 5-10% of cases of MI. Onset 1-3 weeks post MI. Localised pericarditis. Causes fever, pericardial effusions, anaemia, raised ESR, enlarged heart on CXR, pericardial rub (on auscultation). may be similar to PE – another post-MI complication.
It is often self-limiting, and symptoms last a few days.
Treated with NSAID’s, and in more serious cases, steroids.

References

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