How to approach a patient with headache in ED

How to approach a patient with headache in ED

A 30 year old patient comes to the emergency department with history of headache.

How to approach this patient in ED & what important points needs to be evaluated in this patient.

Approach:

-Place the patient on automated BP monitoring ,ECGmonitoring& pulse oximetry
-Vital signs: temperature, blood pressure, pulse, and 02 saturation

Detailed History:

High risk patients:

o Age >50 years, with a new or worsening headache
o Sudden onset of worse severe headache in the life (raises concern for subarachnoid
hemorrhage).
o History of head trauma (even in the last 2 weeks)
o Associated symptoms as:
o Fever, neck stiffness, vomiting and photophobia (raises concern for meningitis)
o Fever and behavior changes (raise concern for encephalitis).
o Confusion, Convulsion or Neurological deficit (raise concern for: stroke or, brain
tumor)
o Vertigo or ataxic gait o Visual changes: Specify _
o Change in headache quality, or progressive headache worsening over
weeks/months
o Medication History (warfarin, and antiplatelet agents) (increase the risk for
intracranial hemorrhage)
o Medication history (chronic steroids or immunosuppressants drugs) (increase risk
of CNSinfections)
o Medication history of oral contraceptive pills (increase risk of venous sinus
thrombosis)
o Pregnant Women: Preeclampsia should be considered in pregnant women after
20th week
o Venous sinus thrombosis should be considered as a cause of headache during
pregnancy, the postpartum state, and hypercoagulation state as (SLE,vasculitis)

Low risk patients:

o Facial pain (raise concern of sinusitis or dental infection)
o Temporal area pain increase with jaw movement (raise concern of temporal
arteritis)
o Medical history as uncontrolled hypertension associated with hypertensive
urgency
o Medication history of nitroglycerin or carbon monoxide poisoning
o History Use of cocaine, amphetamine, and alcohol
o Prior Headache History suggestive of migraine, tension, or cluster-type headaches,
and response to specific therapy
o Family History of aneurysm or sudden death in first-degree relatives (raises the
suspicion for intracranial aneurysm)

DETAILED EXAMINATION:

o Complete Neurologic Examination includes:
o Mental status assessment
o Speech
o Gait
o Pupillary examination (for asymmetry or ptosis)
o Cranial nerve examination
o Motor examination to detect extremity weakness
o Deep tendon reflex examination
o Coordination testing (to detect cerebellar lesions)
o Examination of the Eye: to exclude angle-closure glaucoma or 3rd cranial nerve palsy
o Examine the ears, nose, and throat to identify otitis media and sinusitis
o Examination of the Head and Neck: Meningismus is an important clinical clue to
Meningitis.
o Palpate for tenderness over the temporal arteries to assess for possible temporal
arteritis

Important Differential Diagnosis to consider in ED

1. SUBARACHANOID HEMORRHAGE (SAH)
Following are strongly and reliably associated with SAH

• Sudden onset of headache
• Maximal at onset
• Hx of recent similar headache (Sentinel bleed)
• Age >40
• Neck Stiffness or pain
• Onset of headache on exertion
• Vomiting
• Witnessed loss of consciousness
• Elevated Bp of > 160/100

Also consider the following symptoms

• Stroke like symptoms
• Seizure
• 3rd Cranial Nerve palsy from mass effect
• 6th Cranial Nerve Palsy with diplopa
• Subhyaloid Hemorrhage (Terson Syndrome: Dense red on fundoscopy)
• Meningismus

Risk factors:

• Family history of Cerebral bleed
• History of SAH
• Family history of Polycystic kidney disease
• Collagen vascular disease
• Hypertension
• Binge Drinking
• Use of cocaine or smoking
• Onset of headache during exertion
• Presyncope or syncope with headache

Workup of SAH:

ECG::

• Changes occur in 50-100% of patients due to neurogenic myocardial stunning or coronary vasospasm.
• 
Deep,
wide 
precordial 
T‐wave 
inversion,
 bradycardia,
 and
 prolonged
 QT
• Imp::; don't anticoagulate these patients considering the above findings as ACS

CT Brain:

• Sensitive 95% within 12 hours
• Sensitive 85 % after 1 day
• Sensitive 50% after 1 week

Lumber Puncture:

• Lumber puncture is still standard. However 25% are at increased risk of Post LP headache, Infection and neurological damage.
• Important points to consider for LP here as per recommendations:
• Don't wait till 12 hours after onset for Xanthochromia to be reliably present as then the patient will also be at risk of fatal bleed.
• True positive tap may be hidden in Traumatic tap, so if you wanna say it a true negative tap only if RBC are <5 in tube 4 or a decrease in 25% of RBC from tube 1 to 4.
• Opening pressure should be done as it may be elevated in SAH but will not rise in Traumatic tap, can rise in BIH, CVT
• Post LP headache classically occurs day 3 and are worse when not suppine, are result of CSF leaking from dura or it can be called post dural puncture headache PDPH, which is not shown to be helped with bed rest or caffeine intake but only by Blood patch of patient's own blood. Post LP headache can be minimised by use of smaller needle like 25G and using non cutting needles. (By Dr. Anton)
• If unsuccessful LP or refused by patient then do CT angio to find out if any aneurysm identifiable

Management of SAH:

• Involve Neurosurgeon to consider the target BP if MAP is more than 100-110
• To prevent rebleed treat hypertention if MAP is more than 100 to 110 for few hours and can use IV labetolol 20mg iv bolus then 1-2mg/min infusion not to exceed 300mg or 40-80mg iv q10min with blood pressure monitoring every 5-10min. No dosage alteration in renal or hepatic impaired patients been recommended.
• Oral Nimodipine 60mg p/o or Per NG to prevent vasospasm and subsequent cerebral infarct, every 4-6 hours , should be started within 24hours of presentation. It comes in 30mg gel capsules or 30mg/10ml or 60mg/20ml oral solution. Dosage should be decreased to 30mg in hepatic impairment, closely monitor BP (decreases BP) and HR(arrhythmia).
• Consider starting anti-epileptic which can occur in SAH patients

2. MIGRAINE:

Beware of self diagnosis brought in by patient.

To diagnose as a case of Migraine patient should be diagnosed by physician with history of recurrent similar symptoms with similar intensity and character.

Classical Migraine history will be as follows and can be remembered by Mnemonic of POUND

• Pulsatile quality headache, 4-72Hours duration onset, Unilateral pain, Nausea and Disabling intensity of headache. Can be associated with phono and photophobia. 4 out of 5 features are usually present in POUND Mnemonic.
• Can also present with bilateral colored tunnel vision instead of unilateral flashes and floaters white in color and like a black curtain falling down in cases of vitreous and retinal detachment respectively.
• SSNOOP 
mnemonic
 for 
red 
flags:
 Systemic
 signs
 (fever,
 weight
loss),
 Secondary 
risk
 factors
(immuno‐ compromised 
status,
 HIV),
 Neurological
 signs 
(speech 
deficit,
 cranial 
nerve 
abnormalities),
Onset
–
abrupt,
 Older
age
(>40yo),
Progression
 of 
symptoms (By Dr. Lucas)

Management::

• Inj Metoclopramide 10mg IVI slow infusion over 15-20min or inj prochlorperazine over 15min IVI
• Inj Diphenhydramine 50mg IVI in case of development of extrapyramidal symptoms
• Inj Dexamethasone 10-15mg IV or P/O on discharge (to prevent rebound 72 hrs headache) 
by
decreasing 
the 
inflammation 
of
 the 
blood 
vessels 
in 
the 
brain.
• Naproxen 500mg on discharge shown to be equal effect of Triptans (reported to cause chest tightness), give to people who don't have CVS disease.

3. SPONTANEOUS CERVICAL ARTERY DISSECTION:

Cervical artery dissection is a tear in cervical artery (carotid or vertebral artery) with development of intramural hematoma resulting in stenosis, occlusion or aneurysmal dilation.

Cervical artery dissection usually occurs with minor trauma such as hyperextension of neck during shaving, while driving checking upon blind spot, roller coaster ride, boxing or even coughing in case of connective tissue disease.

Evaluation:

Classic Triad of Carotid Artery Dissection: although only 1/3 of patient present with all 3

• Unilateral pain of head, neck or face
• Partial Horner Syndrome (ptosis, miosis)
• Cerebral or retinal ischemia or TIA symptoms

Dissection of Vertebral artery:

• May present with posterior neck pain
• Headache
• Vertigo
• Ataxia
• Swallowing difficulty

Diagnosis is by:

• CT angiography
• Duplex Scan
• MRA

Management:

• Antithrombotic therapy for at least 3-6 months for a patient with ischemic stroke or TIA
• Endovascular stenting
• Surgical Repair

4. Cerebral Venous Sinus Thrombosis:

Can present in young patients, women more than men.
Symptoms can range from:

• Headache (thunderclap to subacute)
• Seizure
• Stroke like symptoms
• Papilledema, orbital chemosis, proptosis

Risk Factors:

• Thrombophilias
• OCP Use
• Pregnancy
• Malignancy
• Sinusitis 

Evaluation:

• CBC with coagulation profile
• D Dimer (not reliable)
• MRV or CTV(empty delta sign)
• Plain CT (Delta sign, Hemorrhagic infarct  grey white matter junction, hyperdense cervical vein or dural sinus)
• LP may show increased opening pressure

Management:

-Despite risk of hemorrhagic transformation treatment with LMWH or unfractionated heparin shown to reduce Death and dependency.

5. IIH:

Same spectrum of CVT with LP showing increased opening pressure with papilledema and usually young patients, more in females on OCP, but management differs in use of diuretics instead of anticoagulation

6. Carbon monomoxide poisoning:

Multiple patients
Wood burning stove gathering

CT may show bilateral hypodensities

7. Glaucoma: Photophobia, Eye exam mandatory

8: Temporal Arteritis: Other systemic sign and symptoms of disease, PMR, jaw claudication, Blurring of vision, retinal ischemia, check ESR)

9.
Hypertensive encephalopathy ( Altered LOC, Papilledema)

Others::

• Meningitis, encephalitis
• Tumor
• Pre-eclampsia
• Drugs
• Toxins
• Substance abuse, etc

Disclaimer: This don't replace guidelines, follow local protocols.

How to approach a patient with suspected TIA/ Stroke in ED

How to approach a patient with suspected TIA/ Stroke in ED

We know that 10-15% of patient with TIA end up having stroke with up to 50% of these occurring within 48 hours of presentation. 

Time constraint approach

Within 10-15 minutes or less:

• Give Triage Priority with suspected symptoms
• Check vital signs including Bedside glucose determination to rapidly rule out and treat hypoglycemia « 2.8mmoI/L

• Two large caliber(16 gauge or larger) I.V Cannula
• ECG and Cardiac monitoring (look for:::
• A fib (ask about TIA symptoms before thinking to cardiovert patient)
• Crochetage sign (notch in apex of R wave) seen in II, III, aVF is highly specific sign of the presence of a PFO or ASD
• Complete history taking and document time patient last known well 
• Complete neurological examination to exclude other differential
• Complete lab works including CBC, coagulation profile, LFT, U/E & cardiac markers
• NPO

Diagnosis of TIA/Stroke pearls::

• TIA may present with negative symptoms (lack of function), loss of sensory, motor, vision, speech. Common Differentials like Migraine may present with positive symptoms like pain, scotomas, etc.
• Examination of eyes is very important, give regard ti visual field deficits, look for retinal pathology, patients having retinal TIAs need to be worked up same as stroke
• Early signs of stroke on plain CT head (not contraindications to lytic): blurring in basal ganglia, internal capsule or insula; loss of the grey-white junction clarity, sulcal effacement (gyri edema), hyperdense MCA sign has a large differential so exercise caution in ruling in stroke based solely on hyperdense MCA sign 

Within 25 to 30 Min:

• Activate Stoke Team (if available in hospital) and document the time
• Urgent Non Contrast CT Brain
• Chest X ray
• Within 24 hours CT or MRI and vascular imaging (CTA or MRA) from aortic arch to vertex

Within 60min or less:

• Aspirin 324 mg PO (if no hemorrhage in CT brain)
• Labetalol 20mg I.V. 
• If blood pressure above 220/120
• Blood pressure above 185/110 & the patient is eligible for IV tPA (see down)
• Hypertensive Encephalopathy
• Aortic Dissection or MI


• If Hemorrhagic Stroke:
• ED MD secondary survey 
• BP control
• Consider PT/PTT reversal
• Consult Neurosurgery
• NIHSS

• If Ischemic Stroke & within the eligibility: (4.5 hours window) 
• IV tPA (within 60 min) from ERarrival if:
• No contraindications of tPA and within tPA window (4.5 hours) from last well known
• Obtain pre and post tPA NIHSS
• Admit to ICU for 24 hours after tPA infusion.

RISK STRATIFICATION SCORING::

Risk 
stratification 
is 
essential:
 CHADS 
Score 
(CHF,
HTN,
Age>75,
DM,
previous
Stroke)
≥2
 should
 get
 warfarin 
given 
the 
benefits
–
70% 
risk 
reduction 
in 
embolic 
events
–
and 
the 
risks
–
moderate
 bleeds
(10‐12%),
or 
severe
 bleeds
(2‐3%) 
requiring 
hospitalization, 
transfusion, 
or
 causing 
ICH.

Remember
 that 
older 
age 
means 
higher 
risk 
for 
embolic 
event, So older patient will actually get more benefit from warfarin.

INCLUSION & EXCLUSION CRITERIA FOR THROMBOLYTIC THERAPY: 

Administration of Thrombolytic Therapy

Inclusion Criteria: 
Patients presenting within 3 hours of symptoms onset or last seen normal

• Diagnosis of an ischemic stroke causing measurable neurological deficit
• Onset of symptoms is known and is within (3 - 4.5 hours) of the beginning of treatment
• The patient is 18 years age or older

Exclusion Criteria:
Patients presenting within 3 hours

• Significant head trauma or prior stroke within past 3 months
• Symptoms suggest subarachnoid hemorrhage
• Arterial puncture at a non-compressible site in the previous 7 days
• History of previous intracranial hemorrhage
• Intracranial neoplasm, arteriovenous malformation or aneurysm
• Recent intracranial or intraspinal surgery
• Elevated blood pressure that remains higher than 185 mm HG systolic or above 110 diastolic
• Active internal bleeding
• Acute bleeding diathesis, including:
- Platelet count below 100,000/mm3
- Heparin received within last 48 hours that leads to an elevated aPIT
- Current use of Warfarin with INR above 1.7 or PT longer than 15 seconds
- Current use of direct thrombin inhibitors or direct factor with elevated sensitive laboratory tests (such as aPIT)
- INR, platelet count and ecarin clotting time; IT or approximate factor Xa activity assays)
• Blood glucose less than 50 mg/dL
• CT-proven area of multilobar infarct larger than 1/3 total cerebral hemisphere

Relative Exclusion Criteria:
Patients presenting within 3 hours

• Minor or rapidly improving stroke symptoms
• Pregnancy
• Seizure at the onset with postictal residual neurologic impairments
• Major surgery or serious trauma within previous 14 days
• Recent gastrointestinal or urinary tract bleeding in the past 21 days
• Acute MI in the past 3 months.

Inclusion Criteria:
Patients presenting 3 to 4.5 hours from symptoms onset or last seen normal

• Diagnosis of an ischemic stroke causing a measurable neurologic deficit

Relative Exclusion Criteria:
Patients presenting 3 to 4.5 hours from symptoms onset or last seen normal

• Age above 80 years
• Severe stroke with NIHSS score of more than 25
• Patients taking an oral anticoagulant regardless of INR
• Patients with history of both diabetes and prior ischemic stroke

NIH STROKE SCALE SCORING

Disclaimer::
This approach doesn't replace the medical guidelines in any way. Please follow your local guidelines accordingly.

Tricyclic Antidepressants Toxicity

Story goes like this,
A 34 yf has ingested unknown amount of TCA(Tricyclic Antidepressants) ,
The following may be true or false :

1-Pt with prominent anticholinergic toxicity  from TCA poisoning, can benefit  from physostigmine.

False

2-TCAs inhibit the fast sodium channels in the His-Purkinje system and myocardium

True

3-Most seizures are brief and self-limited

True

4-Class IA (eg, procainamide) andClass IC antiarrhythmics (eg, flecainide) can be used for refractory arrhythmias

False

5-ECG changes include R wave in AVR >3 mm; R to S ratio in AVR >0.7 &
Brugada pattern in (15%).

True

6-Consider phenytoin for ventricular dysrhythmias resistant to NaHCO3 and lidocaine and seizures resistant to benzodiazepines.

False

Recommendations:::

●Tricyclic antidepressant (TCA) usage remains common and overdose of TCA medications can be life-threatening. A summary table to facilitate the emergent management of TCA overdose is provided .

●Symptoms and signs of TCA intoxication generally consist of vital sign abnormalities, mental status changes, seizures, and anticholinergic toxicity. Sinus tachycardia and hypotension are common. Sedation is the most typical alteration in mental status, but confusion, delirium, or hallucinations may occur. Anticholinergic toxicity commonly manifests as hyperthermia, flushing, dilated pupils that respond poorly to light, delirium, intestinal ileus, and urinary retention.

●The clinical course of patients with TCA poisoning can be unpredictable, and patients who present immediately after ingestion may initially be well-appearing, only to deteriorate rapidly. Patients must be closely monitored. Maprotiline has been associated with a greater frequency of seizures and arrhythmias than other TCAs.

●Cardiac conduction abnormalities are common in patients with TCA poisoning. These abnormalities can degenerate into ventricular tachycardia and ventricular fibrillation (VT and VF), which occur in approximately 4 percent of TCA overdose cases. The electrocardiogram (ECG) is a most valuable tool in determining the extent of TCA poisoning. The following signs suggest cardiotoxicity:

•Prolongation of the QRS >100 msec

•Abnormal morphology of the QRS (eg, deep, slurred S wave in leads I and AVL)

•Abnormal size and ratio of the R and S waves in lead AVR: R wave in AVR >3 mm; R to S ratio in AVR >0.7

●Although a definitive diagnosis of TCA overdose can be made using serum measurements, such testing is typically not available to clinicians in a timely fashion and seldom plays a role in patient management. Clinically, the diagnosis of TCA poisoning is made based upon a history of ingestion, symptoms and signs consistent with the diagnosis, and characteristic ECG findings.

●Initial treatment of TCA overdose includes assessing and securing the patient’s airway, breathing, and circulation. TCA poisoned patients are frequently moribund and require intubation for airway protection and ventilation. Intravenous boluses of isotonic saline are used to treat hypotension. We recommend sodium bicarbonatetherapy for QRS duration >100 msec or any ventricular arrhythmia caused by TCA poisoning (Grade 1B). The initial dose of sodium bicarbonate is 1 to 2 mEq/kg. In adults, this may be given as two to three 50 mEq (50 mL) vials or prefilled syringes of 8.4 percent sodium bicarbonate given as a rapid IV push through a large bore IV.

●Benzodiazepines remain the treatment of choice for TCA-induced seizures. Reasonable initial treatment options in adults include diazepam 5 mg IV or lorazepam 2 mg IV. Unless bowel obstruction, ileus, or perforation is suspected, we suggest treatment with 1 g/kg of activated charcoal (maximum dose 50 g) in patients who present within two hours of ingestion (Grade 2C). Most patients respond well to standard care; for patients with refractory toxicity, management is reviewed in the text.

●Despite prominent anticholinergic toxicity in some patients, physostigmine is contraindicated as it is associated with cardiac arrest in the setting of TCA toxicity. Class IA (eg, procainamide) andClass IC antiarrhythmics (eg, flecainide) are also contraindicated.

Erythema Multiforme

●Erythema multiforme (EM) is an acute, immune-mediated disorder that involves the skin and/ormucosal surfaces. The treatment of acute EM varies according to the severity of the acute eruption and the presence or absence of recurrent disease.

●Many cases of EM occur secondary to herpes simplex virus (HSV) infection. In patients with HSV-induced EM, treatment with oral antivirals in the acute setting does not alter the course of EM, and is not indicated.

●Most patients with EM can be managed with symptomatic therapy alone. For patients with cutaneous disease and/or mild oral mucosal involvement, treatment with topical corticosteroids, oral antihistamines, and/or an anesthetic mouthwash is sufficient.

●Severe oral mucosal involvement may be accompanied by intense pain and an inability to eat or drink. For patients with severe oral mucosal involvement, we suggest treatment with oral prednisone (40 to 60 mg/day) tapered over the course of two to four weeks (Grade 2C). Patients with disabling symptoms may require hospitalization for nutrition and pain control.

●Ocular involvement rarely may lead to keratitis, conjunctival scarring, or visual impairment. Patients with ocular symptoms should be referred to an ophthalmologist.

●Some patients with EM develop recurrent disease. When feasible, the inciting agent should be identified and eliminated. For patients with HSV-induced or idiopathic EM that recurs ≥6 times per year, or who have fewer, but disabling episodes, we recommend treatment with continuous antiviral therapy (Grade 1B).

●For patients with severe, recurrent EM who fail to respond to continuous systemic antiviral therapy, we suggest treatment with azathioprine, mycophenolate mofetil, or dapsone (Grade 2C). Other options for therapy include other immunomodulatory drugs.

NonSustained Ventricular Tachycardia

Non Sustained V Tachycardia:::

●A variety of definitions of nonsustained ventricular tachycardia (NSVT) have been published, but the most commonly used definition is three or more consecutive ventricular beats, a heart rate of >120 beats per minute, and a duration of arrhythmia of less than 30 seconds.

●Patients with NSVT are usually asymptomatic, although some patients may notice symptoms associated with episodes of NSVT. The type and intensity of symptoms, which may include palpitations, chest pain, shortness of breath, syncope, or presyncope, will vary depending upon the rate and duration of the NSVT along with the presence or absence of significant comorbid conditions.

●Few physical examination findings in patients with NSVT are unique and specific. By definition, patients will have a pulse exceeding 100 beats per minute during the episode. In addition, if the physical examination coincides with an episode of NSVT, this can reveal evidence of atrioventricular (AV) dissociation, including marked fluctuations in blood pressure, variability in the occurrence and intensity of heart sounds (especially S1), and cannon A waves.

●All patients with suspected NSVT should have a 12-lead electrocardiogram (ECG), although NSVT is frequently identified on continuous telemetric monitoring, in which case only one or two leads may be available for review.

●Once nonsustained ventricular tachycardia (NSVT) has been identified, reversible causes of arrhythmia should be sought, including electrolyte imbalances, myocardial ischemia, hypoxia, adverse drug effects, anemia, hypotension, and heart failure. For patients who have only a single asymptomatic episode of NSVT, often no further investigation is required. However, for patients with multiple episodes or for those with symptoms felt to be related to NSVT, a thorough diagnostic evaluation to exclude structural heart disease is warranted, including cardiac imaging and ambulatory ECG monitoring for most patients and invasive electrophysiology studies (EPS) only on rare occasions.

●Treatment of patients with NSVT is as follows:

•Patients with NSVT and no identified symptoms do not require any specific therapy directed toward the NSVT. However, some patients with NSVT who are found to have a cardiomyopathy with significantly reduced left ventricular systolic function may be evaluated for implantable cardioverter defibrillator (ICD) placement for primary prevention of sudden cardiac death related to sustained ventricular tachyarrhythmias.

•For the initial treatment of patients with symptomatic NSVT, we suggest beta blockers rather than calcium channel blockers or antiarrhythmic medications (Grade 2C).

•For patients with NSVT who remain symptomatic in spite of beta blockers, or who are unable to tolerate beta blockers due to side effects, we suggest adding a nondihydropyridine calcium channel blocker (ie, verapamil or diltiazem) rather than an antiarrhythmic medication

•For some patients who have frequent, highly symptomatic NSVT not adequately suppressed by beta blockers or calcium channel blockers, the addition of antiarrhythmic medications (table 1) may be helpful. We suggest amiodarone as the initial choice, rather than other antiarrhythmic drugs, based on its efficacy (Grade 2C).

•In patients who have very frequent, symptomatic monomorphic NSVT not controlled by medications or who are unable or unwilling to take medications, catheter ablation can be effective for reducing or eliminating NSVT and associated symptoms

Some FLASHCARDS in ED: FOAMed worth-sharing

credits: @foampodcast

qSOFA: UPDATED 2017

This is the latest Published article so far:

Sepsis: qSOFA More Accurate Than Previous Criteria in ED
Nicola M. Parry, DVM
January 19, 2017

In the emergency department (ED) setting, the quick Sequential Organ Failure Assessment (qSOFA) score is better than previous criteria for predicting in-hospital mortality among patients with suspected infection, a new study suggests.

Yonathan Freund, MD, PhD, from Pitié-Salpêtrière University Hospital, Paris, France, and colleagues published the results of their multicenter prospective cohort study online January 17 in JAMA.

"Among patients presenting to the [ED] with suspected infection, the use of qSOFA resulted in greater prognostic accuracy for in-hospital mortality than did either SIRS [systemic inflammatory response syndrome] or severe sepsis [criteria]," the authors write.

In 2016, a task force of experts was convened to redefine sepsis in the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). In the previous guideline, the definition of sepsis was based on SIRS criteria, which are nonspecific. In Sepsis-3, the experts redefined sepsis as life-threatening organ dysfunction resulting from a dysregulated host response to infection.

In patients with infection, organ dysfunction is now be identified by an increase in the SOFA score of at least 2 points. The experts recommend that clinicians use qSOFA in settings such as the ED to more rapidly identify patients with sepsis.

Dr Freund and colleagues therefore set out to prospectively validate qSOFA as a mortality predictor in the ED and to compare the accuracy of the new criteria with both the previously used SIRS criteria and the previous definition of severe sepsis (namely, at least two elements of SIRS and a blood lactate level of more than 2 mmol/L (18 mg/dL).

They conducted the study during a 4-week period in 30 EDs in France, Switzerland, Spain, and Belgium, including adult patients with a suspicion of infection who visited the recruiting EDs. Patients were screened and followed until death or hospital discharge.

For each patient, the ED physician recorded the three components of the qSOFA at their worst level during the ED stay (highest respiratory rate, lowest systolic blood pressure, and lowest Glasgow Coma Scale score). The presence of an altered mental status was also recorded independent of Glasgow Coma Scale.

The analysis included 879 patients with a median age of 67 years; 414 (47%) were women. Respiratory tract was the most common site of infection (n = 379; 43%).

"Overall, in-hospital mortality was 8%," the authors note. Patients with a qSOFA score lower than 2 had a 3% mortality rate (95% confidence interval [CI], 2% - 5%), whereas those with a score of 2 or higher had a 24% mortality rate (95% CI, 18% - 30%; absolute difference, 21% [95% CI, 15% - 26%]).

The researchers found qSOFA to be better at predicting in-hospital mortality (area under the receiver operating curve [AUROC], 0.80; 95% CI, 0.74 - 0.85) than the SIRS criteria (AUROC, 0.65; 95% CI, 0.59 - 0.70) and severe sepsis criteria (AUROC, 0.65; 95% CI, 0.59 - 0.70; P < .001 compared with qSOFA).

qSOFA had a sensitivity of 70% (95% CI, 59% - 80%) and specificity of 79% (95% CI, 76% - 82%) for prediction of in-hospital mortality. The test had a positive likelihood ratio of 3.40 (95% CI, 2.80 - 4.17) and a negative predictive value of 97% (95% CI, 95% - 98%).

After adjusting for patient age and site of infection, a qSOFA of 2 or higher was associated with in-hospital mortality with a hazard ratio (HR) of 6.2 (95% CI, 3.8 - 10.3; Harrell C, 0.83). In comparison, using the previous definition of severe sepsis, the HR was 3.5 (95% CI, 2.2 - 5.5).

"One of the strengths of this study is that it prospectively validates the [task force's] findings and highlights how these findings particularly apply to ED patients with even stronger results," the authors conclude.

An accompanying editorial emphasizes the importance of timely identification of patients with possible sepsis.

"[C]linicians must rely on clinical judgment, potentially augmented by clinical criteria validated to identify sepsis among patients with infection," write François Lamontagne, MD, from the University of Sherbrooke, Canada, and David A. Harrison, PhD, and Kathryn M. Rowan, PhD, both from the Intensive Care National Audit & Research Centre, London, United Kingdom.

According to the editorialists, studies have mainly used predictive validity to assess qSOFA. They highlight one particular study of patients with suspected infection that compared use of qSOFA with use of the more complex SOFA or Logistic Organ Dysfunction System tests for patient encounters in hospital settings. In the intensive care unit setting, qSOFA had a worse predictive validity for in-hospital mortality than SOFA or the Logistic Organ Dysfunction System had. However, outside the intensive care unit, qSOFA had a similar or better predictive validity than the other two tests had, despite its relative simplicity.

Although the editorialists acknowledge that qSOFA could therefore be most useful outside the intensive care unit, they stress that the test still needs further evaluation in other settings. For example, in some settings, factors such as how quickly patients with a suspected infection present to the hospital might vary substantially and could affect the test's predictive validity.

Dr Lamontagne and colleagues also suggest that use of qSOFA could be replaced by any highly accurate, rapid diagnostic tests for sepsis that might emerge. However, at least for now, "qSOFA appears a simple, rapid, inexpensive, and valid way to identify — among patients with suspected infection — those at a higher risk of having or developing sepsis," they conclude.

Dr Freund received lecturer fees from Daichi-Sankyo. One coauthor received personal fees from ThermoFisher Brahms, CrossJect, Sanofi, and LFB. Dr Lamontagne served as investigator for a study funded by GlaxoSmithKline and E-Motion, both of which funded remuneration of research staff. The other coauthors and editorialists have disclosed no relevant financial relationships.

JAMA. 2017;317:267-268, 301-308. Article abstract, Editorial extract