A Clinical Guide to the Emergency Department Approach to Headache
Introduction: The Diagnostic Imperative in Acute Headache
Headache is one of the most frequent and challenging complaints encountered in the Emergency Department (ED), accounting for 1-4% of presentations in Malaysia and globally (1). This statistic, however, only hints at the true scale of the issue. Headache disorders are the second leading cause of years lived with disability (YLDs) in Malaysia, representing a profound public health burden that impacts economic productivity and quality of life (3). The core responsibility of the evaluating clinician, therefore, transcends simple diagnosis; it is a high-stakes process of meticulous risk stratification. The primary mandate is not necessarily to provide a definitive sub-specialty diagnosis of a rare primary headache, but to systematically and reliably differentiate a benign, non-life-threatening primary headache from a potentially catastrophic secondary cause (3).
While over 90% of headaches are primary—most commonly migraine or tension-type headache (TTH)—the devastating morbidity and mortality from missed secondary causes like subarachnoid hemorrhage (SAH), meningitis, or cerebral venous thrombosis (CVT) make their exclusion the absolute priority (4). This is especially critical in the ED environment. The patient population presenting to the ED is not a random sample; it is a self-selected group in which usual coping mechanisms and self-management with over-the-counter analgesics have failed (10). This very act of seeking emergency care signifies a headache of unusual severity, a new and frightening character, or the presence of alarming associated symptoms. This selection bias inherently concentrates higher-acuity cases, raising the clinician's pre-test probability of encountering a serious pathology and justifying the thorough, systematic evaluation detailed in this guide (3).
The Clinical Encounter: Assessment and Risk Stratification
A structured history and physical examination are the most powerful diagnostic tools available. In the context of headache, a meticulously obtained history is often more informative than any imaging study, forming the bedrock upon which an accurate diagnosis is built (3, 5).
The Cornerstone: A Structured History
Systematically explore the following features, often called the "headache litany," to build a comprehensive clinical picture:
Onset: Was the onset sudden and explosive, reaching maximum intensity in under a minute? This is a "thunderclap" headache, the single most alarming feature in a headache history. It is caused by the sudden stretching of pain-sensitive structures like the meninges, often from an arterial bleed, and must be considered a subarachnoid hemorrhage until proven otherwise (50). Contrast this with a headache that builds gradually over minutes to hours, which is more typical of primary headaches or other secondary causes like meningitis.
Frequency and Duration: How often do the headaches occur, and how long does a typical attack last? This temporal pattern is key. For example, cluster headache attacks are brief (15-180 minutes) but can occur multiple times a day, whereas a migraine attack typically lasts for many hours to a few days (3). A crucial red flag is a change in a previously stable pattern—for instance, a patient with known episodic migraine who now describes a new, unremitting daily headache. This progression demands investigation (3).
Location: Is the pain unilateral or bilateral? Strictly unilateral pain is a classic feature of migraine and is required for the diagnosis of cluster headache. Bilateral, "band-like" pain is the hallmark of TTH (23). However, be aware that migraine can sometimes present bilaterally, and pain localized to the occipital region should raise suspicion for posterior fossa pathology.
Character: The patient's description of the pain is highly informative. Is it a deep, intense throbbing or pulsating, like a heartbeat in the head (suggestive of the vasodilation component in migraine)? Is it a dull, persistent, pressing or tightening sensation, often described as a "tight cap" or "band around the head" (TTH)? Or is it an excruciatingly sharp, stabbing, or boring pain, often described as a "hot poker in the eye" (cluster headache)? (3)
Severity: Use a 1-10 pain scale to quantify severity and track treatment response. The description of a headache as the "worst headache of my life" is a classic, albeit non-specific, red flag that demands immediate and serious consideration of SAH (26).
Associated Symptoms: The presence or absence of associated symptoms often clinches a diagnosis.
Gastrointestinal/Sensory: Nausea, vomiting, photophobia (light sensitivity), and phonophobia (sound sensitivity) are cardinal features of migraine. Their presence is thought to result from the activation of brainstem centers, like the dorsal raphe nucleus and locus coeruleus, by the same trigeminovascular pathways that drive the pain (50).
Systemic: The presence of fever, neck stiffness, or a non-blanching rash are systemic signs that demand immediate consideration of a central nervous system infection like meningitis or encephalitis (51).
Autonomic: A red, tearing eye (conjunctival injection/lacrimation), runny or blocked nose (rhinorrhea/congestion), or a drooping eyelid (ptosis) on the same side as the pain are pathognomonic for trigeminal autonomic cephalalgias (TACs). Their presence reflects the activation of the trigeminal-autonomic reflex via the parasympathetic pathway (36).
Aggravating/Alleviating Factors:
Activity: Migraine is characteristically worsened by routine physical activity like walking or climbing stairs, forcing the patient to seek rest. TTH is typically not aggravated by such activity (25).
Position: A headache that is significantly worse when standing up and relieved by lying down is the hallmark of low CSF pressure (e.g., from a post-LP leak). This is caused by the downward sagging of intracranial structures, which tugs on the pain-sensitive meninges. Conversely, a headache that is worse when lying flat and aggravated by coughing, straining, or bending over (Valsalva maneuver) suggests raised intracranial pressure (ICP) (3).
Risk Factors: Inquire about systemic illness (cancer, HIV, autoimmune disease), recent trauma (even minor neck injuries can cause arterial dissection), medication use (especially anticoagulants, oral contraceptives, and regular use of analgesics, which can lead to medication overuse headache), and a detailed family history of similar headaches (51).
The Physical and Neurological Examination
A focused but thorough physical examination is mandatory for every patient presenting with a headache to identify signs of underlying structural pathology.
Vital Signs: Check for fever (infection), marked hypertension (hypertensive emergency, PRES, SAH), or tachycardia and hypotension (sepsis, dehydration) (30).
Funduscopy: This is a non-negotiable and essential clinical skill. The presence of papilledema (swelling of the optic disc, seen as blurred disc margins and loss of the physiological cup) is a direct sign of raised ICP and is a major red flag for conditions like a brain tumor, IIH, or CVT. The absence of spontaneous venous pulsations can be an earlier, more subtle sign of raised ICP (24).
Meningeal Signs: Test for neck stiffness (nuchal rigidity). While positive Kernig's or Brudzinski's signs are specific for meningeal irritation, they are not perfectly sensitive and may be absent in early meningitis, or in elderly or immunocompromised patients (5).
Neurological Examination: A comprehensive neurological exam is critical. Any new focal neurological deficit is a major red flag mandating urgent neuroimaging. This includes subtle weakness, sensory loss, dysphasia, ataxia, or cranial nerve palsies. For example, a third nerve palsy presenting with a fixed, dilated pupil ("blown pupil") can indicate compression by an expanding posterior communicating artery aneurysm (24, 52).
Head and Neck: Palpate the pericranial muscles for tenderness, which is common in TTH. In patients over 50, carefully palpate the temporal arteries for tenderness, thickening, or a reduced pulse, which are key signs of Giant Cell Arteritis (GCA) (24).
Identifying High-Risk Patients: The SNNOOP10 Red Flags
The SNNOOP10 mnemonic is an internationally recognized and validated tool to help clinicians remember critical features that increase the likelihood of a serious secondary cause for a headache (1). The presence of one or more of these flags is the primary indication for further investigation.
Systemic symptoms (fever, chills, weight loss) or Secondary risk factors (HIV, cancer, immunosuppression)
Neoplasm history (primary brain tumor or metastasis)
Neurologic deficit (any new focal finding, including confusion or altered consciousness)
Onset is sudden or abrupt (a "thunderclap" headache peaking in <1 minute)
Older age (new onset or new pattern of headache after age 50)
Pattern change or Progressive headache (change in frequency, severity, or features)
Positional headache (worse when standing or lying down)
Precipitated by sneezing, coughing, or exertion (Valsalva maneuver)
Papilledema (visual sign of raised ICP)
Pregnancy or puerperium (increased risk of CVT, pre-eclampsia)
Painful eye with autonomic features (risk of acute glaucoma, cavernous sinus pathology)
Post-traumatic onset of headache
Pathology of the immune system (known immunodeficiency)
Painkiller overuse (risk of Medication Overuse Headache)
It is crucial to understand that red flags are tools for risk stratification, not definitive diagnostic criteria. While they are sensitive for serious pathology, their specificity can be low. The clinician's role is not simply to tick boxes, but to synthesize the entire clinical picture. The presence of multiple red flags, or a single high-risk flag (like a new focal deficit) in a patient with relevant risk factors, dramatically increases the pre-test probability of a secondary cause and lowers the threshold for immediate, aggressive investigation (1).
Differential Diagnosis: Pattern Recognition
After risk stratification, the clinician can focus on pattern recognition to formulate a differential diagnosis. Intimate knowledge of the features of common primary headaches is essential to distinguish them from their critical secondary mimics.
The "Usual Suspects": Common Primary Headaches
Migraine: This is a complex neurological disorder, not just a headache. It often presents as a unilateral, pulsating headache lasting 4-72 hours, aggravated by routine activity, and associated with nausea/vomiting or photophobia/phonophobia. Patients characteristically seek refuge in a dark, quiet room (50, 53). Many patients experience distinct phases: a premonitory phase (hours to days before), aura (transient neurological symptoms, usually visual), the headache itself, and a postdrome phase of fatigue and cognitive fogginess.
Tension-Type Headache (TTH): This is the most prevalent primary headache. It is defined by what it lacks as much as by what it possesses. It presents as a bilateral, non-pulsating, pressing or tightening pain of mild-to-moderate intensity that is not aggravated by activity. There is no nausea or vomiting, and only one of photophobia or phonophobia may be present, but not both (23). The underlying mechanism is thought to involve peripheral sensitization of myofascial nociceptors in the episodic form, and central sensitization within the trigeminal pathways in the chronic form.
Cluster Headache: This is the most common of the trigeminal autonomic cephalalgias and is arguably the most painful condition known to medicine, sometimes termed "suicide headache." Attacks are defined by their brevity (15-180 minutes) and excruciating intensity. The pain is severe, strictly unilateral, and localized to the orbital or temporal region. It is always accompanied by prominent same-sided autonomic features (red/tearing eye, runny nose) and a profound sense of restlessness or agitation, causing patients to pace or rock (36, 38). The striking circadian and circannual periodicity strongly implicates the hypothalamus in its pathophysiology.
The "Must-Not-Miss": Critical Secondary Headaches
Subarachnoid Hemorrhage (SAH): The hallmark is a thunderclap headache, often described as being "hit in the head with a baseball bat." It may be associated with a transient loss of consciousness, seizure, vomiting, or photophobia. Neck stiffness (meningism) may not be present immediately but typically develops within 24 hours as the blood irritates the meninges (26, 27). Be aware of "sentinel headaches," which are smaller, warning leaks that can precede a major rupture by days or weeks.
Meningitis/Encephalitis: The clinical presentation is that of an acute febrile illness. The headache is typically severe, generalized, and unremitting. The classic diagnostic triad consists of fever, neck stiffness (nuchal rigidity), and altered mental status, although it is important to note that fewer than half of patients present with all three features (28). The presence of a non-blanching petechial or purpuric rash is a highly specific sign for meningococcal septicemia and constitutes a medical emergency.
Cerebral Venous Thrombosis (CVT): CVT is a notorious diagnostic chameleon and "the great mimicker." Headache is the most frequent symptom (up to 90% of cases), but it has no single characteristic pattern. It can be diffuse or unilateral, gradual and progressive, or present as a thunderclap headache. The key to suspicion is the clinical context. The headache is often associated with other signs of neurological dysfunction, such as focal deficits, seizures, or signs of raised ICP (papilledema). The diagnosis should be strongly considered in patients with a prothrombotic state, particularly young women who are pregnant, postpartum, or using oral contraceptives (43, 61).
Giant Cell Arteritis (GCA): This diagnosis is a medical emergency and must be considered in any patient over the age of 50 presenting with a new-onset headache. The headache is typically unilateral and localized to the temporal region. The most specific associated features are jaw claudication (pain or fatigue in the jaw muscles with chewing) and visual symptoms (from transient blurring to sudden, permanent vision loss due to ischemic optic neuropathy). Prompt treatment with high-dose steroids is essential to prevent irreversible blindness (5).
The Diagnostic Pathway: Judicious Investigations
The decision to investigate is one of the most critical junctures in management. The guiding principle is judicious use: tests should be ordered to answer a specific clinical question, primarily to rule out a suspected secondary cause in a patient with red flag features. For a patient with a long-standing, stable headache pattern that meets ICHD-3 criteria for a primary headache and has no red flags, neuroimaging is generally not indicated (5, 53).
Laboratory Tests: There is no standard panel. Investigations should be targeted. Order a Full Blood Count (FBC) and C-Reactive Protein (CRP) if infection is suspected. An Erythrocyte Sedimentation Rate (ESR) and CRP are mandatory first-line tests if GCA is suspected in a patient over 50 (30, 51).
Non-Contrast CT (NCCT) Head: For most emergent headache evaluations, the NCCT is the initial imaging test of choice. It is fast, widely available, and highly effective at answering the most immediate, life-threatening question: is there blood? It can also readily identify significant mass effect, midline shift, hydrocephalus, or large tumors (52).
Specific Diagnostic Scenarios
The Thunderclap Headache (Suspected SAH)
This specific presentation mandates a strict and evidence-based diagnostic algorithm:
Emergency NCCT Head: The sensitivity of modern multi-slice CT scanners for detecting SAH approaches 100% if the scan is performed within 6 hours of symptom onset. This "6-hour rule" is a fundamental concept, based on the rate at which hemoglobin breaks down and becomes less visible (isodense) on CT (57).
Lumbar Puncture (LP): If the NCCT is negative but clinical suspicion for SAH remains high (especially if the patient presents more than 6 hours after onset), an LP is the mandatory next step. The CSF is analyzed for opening pressure and the presence of xanthochromia (the yellowish discoloration of the supernatant after centrifugation). Xanthochromia is the pathognomonic finding, as it takes 6-12 hours to develop and definitively proves that blood has been in the CSF for some time, ruling out a simple traumatic tap (26, 50).
CT Angiography (CTA): This is often performed immediately after the initial NCCT. Its role is to identify the source of the bleeding, typically a ruptured aneurysm, and to guide definitive neurosurgical or endovascular treatment (26).
Suspected Meningitis
Immediate Action: The mantra is "treat before you tap/scan" if there are any signs of significantly raised ICP (papilledema, new focal deficit, severely altered consciousness). In this scenario, do not delay treatment. Draw blood cultures, administer empiric IV antibiotics and dexamethasone, and then send the patient for a CT head to rule out a mass lesion before performing an LP (30). Delaying antibiotics to obtain a "pure" CSF culture can have devastating consequences.
Lumbar Puncture: If there are no signs of raised ICP, proceed directly to LP. CSF analysis is the definitive diagnostic test. Typical findings in bacterial meningitis are a high opening pressure, turbid appearance, high white cell count (predominantly neutrophils), an elevated protein level, and a low glucose level (CSF:serum ratio <0.4) (30).
Management in the Malaysian ED
Treatment must be prompt, effective, and guided by local protocols. For a patient presenting with severe pain (score ≥7), the MOH Pain Management Guidelines state that appropriate analgesia should be administered within 20 minutes of arrival (74).
Acute Primary Headache Management
Migraine: A Multimodal Abortive Strategy
A combination approach targeting multiple pathophysiological pathways is most effective. The goal is to terminate the attack quickly and prevent recurrence (75):
Parenteral NSAID: IV/IM Ketorolac 30-60 mg to target neurogenic inflammation.
Antiemetic/Dopamine Antagonist: IV Metoclopramide 10 mg or IV Prochlorperazine 10 mg. These agents are crucial, serving a dual purpose: they treat associated nausea and have a primary headache-aborting effect by acting on dopamine receptors in the brainstem.
Prevent Akathisia: Co-administer IV Diphenhydramine 25-50 mg with the antiemetic to block the distressing extrapyramidal side effects.
Hydration: 1L IV Normal Saline, as many patients are dehydrated from vomiting, which can itself perpetuate the headache.
Prevent Recurrence: A single dose of IV Dexamethasone 10 mg has been shown to significantly reduce the rate of headache recurrence within 24-72 hours.
Note: The use of opioids (e.g., tramadol, pethidine) for primary headache is strongly discouraged. They are less effective than migraine-specific therapies, are associated with higher rates of rebound headache and return ED visits, and carry a significant risk of tolerance, dependence, and progression to medication overuse headache (8).
Tension-Type Headache
First-line: Simple analgesics like Paracetamol 1g or oral NSAIDs are usually sufficient (80).
Severe TTH: For patients presenting with severe, refractory TTH, a parenteral NSAID such as IV/IM Ketorolac 30 mg can be effective (6).
Cluster Headache
Management is unique and must be rapid-acting due to the short but excruciating nature of the attacks:
High-Flow Oxygen: This is the safest and one of the most effective first-line treatments. It is essential that it is administered correctly: 100% oxygen via a non-rebreathing face mask at a high flow rate of 12-15 L/min for 15-20 minutes. The patient should be sitting upright. The proposed mechanism is cerebral vasoconstriction and modulation of brainstem centers (3).
Pharmacotherapy: Fast-acting subcutaneous or intranasal triptans are the most effective pharmacological treatments but are not currently available in the Malaysian market. This presents a significant management challenge. In their absence, the MSN guidelines suggest that IV/IM Tramadol 50-100 mg may be useful in the ED setting (3).
Initial Management of Life-Threatening Secondary Headaches
Subarachnoid Hemorrhage: Once diagnosed, this is a neurosurgical emergency. Key interventions include immediate neurosurgical consultation, aggressive blood pressure control (target SBP <160 mmHg) with a titratable IV agent like Nicardipine, and initiation of oral Nimodipine to prevent delayed cerebral ischemia from vasospasm (26, 68).
Bacterial Meningitis: This is a time-critical medical emergency. After blood cultures have been drawn, immediately start empiric, bactericidal antibiotics that achieve good CSF penetration. A standard regimen is IV Ceftriaxone 2g BD plus IV Vancomycin (to cover for resistant S. pneumoniae). Give IV Dexamethasone 10 mg just before or with the first antibiotic dose to reduce inflammation and the risk of neurological sequelae (30).
Disposition: Admission vs. Safe Discharge
The decision to admit or discharge is a final, critical step that hinges on diagnostic certainty and patient safety.
Admission Criteria: All patients with a confirmed or highly suspected serious secondary headache must be admitted for definitive treatment and monitoring. For patients with primary headaches, admission is warranted for those with intractable pain despite aggressive ED treatment (a condition known as status migrainosus), persistent nausea and vomiting requiring ongoing IV hydration, or those with red flag features who cannot be fully and safely investigated and cleared in the ED.
Safe Discharge Planning: For the majority of patients with primary headaches who respond well to treatment, a safe and effective discharge plan is crucial to prevent early re-attendance and empower the patient. This plan must include:
Clear Patient Education: A simple, clear explanation of the diagnosis (e.g., "You have migraine, which is a neurological condition, not a dangerous brain problem"), reassurance, and practical advice on identifying and avoiding personal triggers (34).
Rescue Medication: A prescription for appropriate oral abortive medication (e.g., an NSAID and an antiemetic for migraine) with clear instructions on when and how to take it.
Explicit Follow-up: A clear plan for follow-up with a General Practitioner (GP), a primary care clinic (Klinik Kesihatan), or a referral to a neurology clinic for consideration of preventive therapy. Providing the patient with a simple headache diary is a valuable tool to facilitate this follow-up and improve long-term management (6, 89).
Specific Return Advice: Provide clear, actionable triggers for when to return to the ED (e.g., "if the headache is the worst of your life," "if you develop a fever, neck stiffness, or weakness," or "if the headache is different from your usual pattern").
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