Type 2 Diabetes Mellitus (T2DM)

A 52-year-old man with obesity presents with a 4-month history of progressive fatigue, increased thirst, frequent urination, and intermittent blurred vision. He also reports increased appetite but no significant weight loss. His medical history includes hypertension and dyslipidemia, and his father has type 2 diabetes mellitus. He has a sedentary lifestyle. On examination, BMI is 33 kg/m², blood pressure is 146/86 mm Hg, and there is central adiposity with acanthosis nigricans over the posterior neck. Laboratory investigations show a fasting plasma glucose of 156 mg/dL and an HbA1c of 8.2%. Serum creatinine and eGFR are normal. Diagnosis?

Diagnosis is Type 2 Diabetes Mellitus (T2DM).

1. Definition

Type 2 diabetes mellitus is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic beta-cell dysfunction, resulting in persistent hyperglycemia.

It is the most common form of diabetes mellitus.

2. Epidemiology

1.      T2DM accounts for the majority of diabetes cases worldwide

2.      Its prevalence increases with overweight, obesity, physical inactivity, and advancing age

3.      It has a strong genetic and familial predisposition

4.      It is increasingly diagnosed in younger adults and adolescents

3. Pathophysiology

1.      Peripheral insulin resistance develops in skeletal muscle and adipose tissue

2.      The pancreas initially compensates with increased insulin secretion

3.      Progressive beta-cell dysfunction reduces insulin secretion

4.      Hepatic glucose production increases

5.      Persistent hyperglycemia develops

6.      Chronic hyperglycemia and associated metabolic abnormalities contribute to microvascular and macrovascular complications

4. Risk Factors

1.      Overweight or obesity

2.      Physical inactivity

3.      Family history of diabetes

4.      Increasing age

5.      Hypertension

6.      Dyslipidemia

7.      History of gestational diabetes

8.      Polycystic ovary syndrome

9.      Cardiovascular disease

10.  Other conditions associated with insulin resistance

5. Clinical Features

5.1 Classic Hyperglycemic Symptoms

1.      Polyuria

2.      Polydipsia

3.      Polyphagia

4.      Fatigue

5.      Blurred vision

6.      Unintentional weight loss may occur with more severe hyperglycemia

5.2 Signs of Insulin Resistance

1.      Central obesity

2.      Acanthosis nigricans

5.3 Features Suggesting Complications

1.      Recurrent infections

2.      Peripheral neuropathic symptoms

3.      Foot ulcers

4.      Erectile dysfunction

5.      Visual impairment

6.      Symptoms of cardiovascular or peripheral arterial disease

6. Screening

1.      Screening for prediabetes and T2DM should begin at age 35 years for adults without other indications for earlier testing

2.      Screen adults of any age with overweight or obesity and one or more additional diabetes risk factors

3.      People with prediabetes should generally be tested yearly

4.      If screening is normal, repeat testing at least every 3 years, or sooner depending on symptoms and risk factors

7. Diagnosis

Diabetes is diagnosed by any of the following:

1.      HbA1c ≥6.5%

2.      Fasting plasma glucose ≥126 mg/dL

3.      2-hour plasma glucose ≥200 mg/dL during a 75-g oral glucose tolerance test

4.      Random plasma glucose ≥200 mg/dL in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis

In the absence of unequivocal hyperglycemia, two abnormal test results are required for confirmation. These may be two different abnormal tests obtained at the same time or at different times, or the same abnormal test repeated.

This patient has both a fasting plasma glucose of 156 mg/dL and an HbA1c of 8.2%, so the diagnosis of diabetes is confirmed.

7.1 Prediabetes

1.      HbA1c: 5.7 to 6.4%

2.      Fasting plasma glucose: 100 to 125 mg/dL

3.      2-hour plasma glucose: 140 to 199 mg/dL during a 75-g OGTT

8. Initial Evaluation

8.1 History

1.      Hyperglycemic symptoms

2.      Duration and severity of symptoms

3.      Family history of diabetes and cardiovascular disease

4.      Diet and physical activity

5.      Medication review

6.      Cardiovascular and renal history

7.      Smoking and alcohol history

8.      Symptoms of neuropathy, retinopathy, or peripheral arterial disease

8.2 Examination

1.      BMI and weight

2.      Blood pressure

3.      Signs of insulin resistance

4.      Cardiovascular examination

5.      Comprehensive foot examination

6.      Assessment for peripheral neuropathy

8.3 Baseline Investigations

1.      HbA1c

2.      Serum creatinine and eGFR

3.      Urine albumin-to-creatinine ratio (UACR)

4.      Lipid profile

5.      Liver biochemical tests when clinically appropriate

6.      Additional testing for alternative or secondary causes of diabetes when indicated

9. Complications

9.1 Microvascular Complications

1.      Diabetic retinopathy

2.      Diabetic kidney disease

3.      Diabetic peripheral and autonomic neuropathy

9.2 Macrovascular Complications

1.      Coronary artery disease

2.      Cerebrovascular disease

3.      Peripheral arterial disease

9.3 Acute Complications

1.      Hyperosmolar hyperglycemic state (HHS)

2.      Diabetic ketoacidosis (DKA) can occur in T2DM, although it is less typical

3.      Hypoglycemia related to glucose-lowering therapy

10. Glycemic Targets

10.1 Most Nonpregnant Adults

1.      An HbA1c target <7% is appropriate for many adults

2.      Glycemic targets should be individualized

10.2 More Stringent Targets

An HbA1c target such as <6.5% may be appropriate when safely achievable in selected patients with:

1.      Good overall health and function

2.      Low hypoglycemia risk

3.      Low treatment burden

4.      Few significant comorbidities

10.3 Less Stringent Targets

Less stringent targets may be appropriate in patients with:

1.      Significant comorbidity

2.      Frailty

3.      Cognitive or functional impairment

4.      High hypoglycemia risk

5.      Greater treatment burden than expected benefit

11. Management

11.1 Lifestyle and Weight Management

Lifestyle intervention is recommended for all patients.

1.      Use an individualized, nutritionally balanced eating pattern emphasizing minimally processed and nutrient-dense foods

2.      Reduce excess caloric intake and refined carbohydrates when appropriate

3.      Encourage weight reduction in patients with overweight or obesity

4.      Aim for at least 150 minutes per week of moderate-to-vigorous aerobic activity, spread over at least 3 days

5.      Perform resistance exercise 2 to 3 times per week

6.      Reduce prolonged sedentary behavior

Weight reduction improves glycemic control and overall cardiometabolic risk.

11.2 Pharmacologic Therapy

Medication selection should be individualized according to:

1.      Glycemic effectiveness

2.      Obesity and weight goals

3.      Atherosclerotic cardiovascular disease or high cardiovascular risk

4.      Heart failure

5.      Chronic kidney disease

6.      Hypoglycemia risk

7.      Adverse effects

8.      Cost and access

9.      Patient preference

Metformin

1.      Metformin remains a commonly used initial glucose-lowering medication when appropriate

2.      It is effective, inexpensive, and has a low risk of hypoglycemia

3.      It is generally weight neutral or may produce modest weight loss

4.      Do not initiate metformin when eGFR is <45 mL/min/1.73 m²

5.      In patients already taking metformin, reduce or reassess the dose when eGFR falls below 45 mL/min/1.73 m²

6.      Discontinue metformin when eGFR is <30 mL/min/1.73 m²

7.      Long-term use may be associated with vitamin B12 deficiency

GLP-1 Receptor Agonists and Dual GIP/GLP-1 Receptor Agonists

1.      Particularly useful in patients with T2DM and overweight or obesity

2.      Agents such as semaglutide and tirzepatide have high weight-loss efficacy

3.      GLP-1 receptor agonists with demonstrated cardiovascular benefit should be prioritized when appropriate in patients with established or high-risk ASCVD

4.      These therapies have a low intrinsic risk of hypoglycemia unless combined with insulin or insulin secretagogues

SGLT2 Inhibitors

1.      Particularly important in patients with heart failure or chronic kidney disease

2.      Provide cardiovascular and renal protection in appropriate patients

3.      Benefits for heart failure and CKD may justify use irrespective of HbA1c

4.      Important adverse effects include genital mycotic infections and volume depletion

5.      Rare euglycemic DKA may occur

Other Options

1.      DPP-4 inhibitors

2.      Sulfonylureas

3.      Thiazolidinediones

4.      Insulin

For this patient, lifestyle and weight-management therapy should begin immediately. Pharmacologic therapy is also indicated. Metformin is a reasonable option because renal function is normal. A GLP-1 receptor agonist or dual GIP/GLP-1 receptor agonist is particularly attractive when substantial weight loss is a major treatment goal. Because he has symptoms of hyperglycemia, insulin may be considered, but his HbA1c of 8.2% and fasting glucose of 156 mg/dL do not by themselves mandate insulin therapy in the absence of severe hyperglycemia, catabolic features, or hyperglycemic crisis.

11.3 When to Consider Insulin

Insulin should be considered when:

1.      Symptoms of hyperglycemia are present

2.      HbA1c >10%

3.      Blood glucose is ≥300 mg/dL

4.      Catabolic features are present, such as unexplained weight loss or ketosis

5.      There is a hyperglycemic crisis

In adults with T2DM without evidence of severe insulin deficiency, severe hyperglycemia, or hyperglycemic crisis, GLP-1-based therapy is generally preferred to insulin as initial or add-on injectable therapy.

12. Monitoring and Complication Screening

12.1 Glycemic Monitoring

1.      Assess HbA1c approximately every 3 months when glycemic goals are not being met or treatment has recently changed

2.      Once stable and at goal, assess glycemic status at least twice yearly

12.2 Retinopathy

1.      Perform a dilated comprehensive eye examination at the time of diagnosis of T2DM

2.      If examinations remain normal and glycemia is controlled, screening every 1 to 2 years may be considered

3.      Retinopathy requires at least annual or more frequent follow-up depending on severity

12.3 Kidney Disease

1.      Assess UACR and eGFR at least annually in all patients with T2DM

2.      Monitor more frequently when CKD is present

12.4 Neuropathy and Foot Care

1.      Assess for peripheral neuropathy at diagnosis and at least annually

2.      Perform 10-g monofilament testing annually to identify feet at risk for ulceration and amputation

3.      Perform a comprehensive foot examination at least annually

4.      Inspect the feet at every visit in patients with sensory loss or a history of ulceration or amputation

13. Cardiovascular and Renal Protection

1.      Optimize blood pressure control

2.      Treat dyslipidemia with appropriate statin therapy

3.      Encourage smoking cessation

4.      Use an ACE inhibitor or ARB when indicated, particularly in patients with hypertension and albuminuria

5.      Use SGLT2 inhibitors in appropriate patients with CKD or heart failure

6.      Use GLP-1 receptor agonists with demonstrated cardiovascular benefit in appropriate patients with established or high-risk ASCVD

7.      Maintain age-appropriate vaccination

8.      Address obesity as an important component of cardiovascular risk reduction

Because this patient is 52 years old with diabetes and additional ASCVD risk factors, including hypertension and dyslipidemia, high-intensity statin therapy is recommended if tolerated, with a goal of reducing LDL cholesterol by at least 50% from baseline and achieving an LDL cholesterol level <70 mg/dL for primary prevention.

14. Key Clinical Insight

Obesity + polyuria + polydipsia + acanthosis nigricans + elevated fasting glucose and HbA1c strongly indicate type 2 diabetes mellitus with insulin resistance.

Fasting plasma glucose ≥126 mg/dL or HbA1c ≥6.5% meets a diagnostic threshold for diabetes. In the absence of unequivocal hyperglycemia, two abnormal results confirm the diagnosis.

Management should address not only glycemia but also weight, cardiovascular risk, kidney protection, blood pressure, and dyslipidemia.

References

1.      American Diabetes Association Professional Practice Committee for Diabetes. 2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes 2026. Diabetes Care. 2026;49(Suppl 1):S27-S49. doi:10.2337/dc26-S002.

2.      American Diabetes Association Professional Practice Committee for Diabetes. 5. Facilitating Positive Health Behaviors and Well-being to Improve Health Outcomes: Standards of Care in Diabetes 2026. Diabetes Care. 2026;49(Suppl 1):S89-S131. doi:10.2337/dc26-S005.

3.      American Diabetes Association Professional Practice Committee for Diabetes. 6. Glycemic Goals, Hypoglycemia, and Hyperglycemic Crises: Standards of Care in Diabetes 2026. Diabetes Care. 2026;49(Suppl 1):S132-S149. doi:10.2337/dc26-S006.

4.      American Diabetes Association Professional Practice Committee for Diabetes. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes 2026. Diabetes Care. 2026;49(Suppl 1):S183-S215. doi:10.2337/dc26-S009.

5.      American Diabetes Association Professional Practice Committee for Diabetes. 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes 2026. Diabetes Care. 2026;49(Suppl 1):S216-S245. doi:10.2337/dc26-S010.

6.      American Diabetes Association Professional Practice Committee for Diabetes. 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes 2026. Diabetes Care. 2026;49(Suppl 1):S246-S260. doi:10.2337/dc26-S011.

7.      American Diabetes Association Professional Practice Committee for Diabetes. 12. Retinopathy, Neuropathy, and Foot Care: Standards of Care in Diabetes 2026. Diabetes Care. 2026;49(Suppl 1):S261-S276. doi:10.2337/dc26-S012.

Subarachnoid Hemorrhage (SAH)

A 46-year-old female presents to the emergency department with sudden onset of the worst headache of her life that reached maximal intensity within seconds while exercising. She reports nausea, vomiting, photophobia, and neck stiffness. She denies previous similar headaches. Blood pressure is 165/95 mm Hg, heart rate is 96 beats per minute, and she is alert and oriented. Neurologic examination shows no focal deficit. Noncontrast head CT demonstrates acute subarachnoid blood within the basal cisterns and sylvian fissures. Diagnosis?

Diagnosis is Acute Subarachnoid Hemorrhage (SAH).

1. Initial Approach to Acute Headache

The priority in a patient with acute headache is to identify dangerous secondary causes before diagnosing a primary headache disorder.

A practical approach is:

STABILIZE → IDENTIFY RED FLAGS → PRIMARY vs SECONDARY → DEFINE PHENOTYPE → TARGETED TESTING → TREAT THE CAUSE

A normal neurologic examination does not exclude serious secondary headache, including SAH.

2. Headache Red Flags: SNOOP+

2.1 Systemic Features

1.      Fever

2.      Unintentional weight loss

3.      Known malignancy

4.      Immunosuppression

5.      Pregnancy or postpartum state

6.      Systemic inflammatory or infectious disease

2.2 Neurologic Features

1.      Focal neurologic deficit

2.      Altered mental status

3.      Seizure

4.      Papilledema

5.      Persistent visual loss

2.3 Sudden Onset

1.      Thunderclap headache reaches maximal intensity within approximately 1 minute

2.      A new thunderclap headache requires urgent evaluation for a secondary vascular cause

2.4 Older Age

New headache beginning after approximately 50 years of age should raise concern for causes such as:

1.      Giant cell arteritis

2.      Malignancy

3.      Structural intracranial disease

2.5 Pattern Change

Important features include:

1.      First or worst headache

2.      Progressively worsening headache

3.      New headache phenotype

4.      Increasing frequency or severity

2.6 Additional Red Flags

1.      Positional headache

2.      Triggered by cough, Valsalva, exertion, or sexual activity

3.      Recent trauma

4.      Anticoagulant use

5.      Painful red eye

6.      New headache during pregnancy or postpartum

3. Thunderclap Headache

A thunderclap headache should prompt urgent evaluation for subarachnoid hemorrhage until adequately excluded.

Important differential diagnoses include:

1.      Subarachnoid hemorrhage

2.      Reversible cerebral vasoconstriction syndrome (RCVS)

3.      Cerebral venous sinus thrombosis (CVST)

4.      Cervical artery dissection

5.      Pituitary apoplexy

6.      Intracerebral hemorrhage

A normal neurologic examination does not exclude SAH.

4. Subarachnoid Hemorrhage

4.1 Clinical Features

Typical features include:

1.      Sudden severe thunderclap headache

2.      Headache reaching maximal intensity rapidly

3.      Nausea and vomiting

4.      Neck stiffness or meningismus

5.      Photophobia

6.      Transient or persistent loss of consciousness

7.      Seizure

8.      Focal neurologic deficits may occur but can be absent

A patient may therefore have SAH despite being awake, neurologically intact, and hemodynamically stable.

4.2 Initial Diagnostic Test

The initial investigation for suspected SAH is:

Noncontrast head CT

Presentation within 6 hours

In an appropriately selected neurologically intact patient with nontraumatic headache, a normal high-quality noncontrast head CT performed within 6 hours of symptom onset can rule out SAH when imaging quality and interpretation are adequate.

If clinical suspicion remains high despite a negative CT, additional evaluation remains appropriate.

Presentation ≥6 hours or new neurologic deficit

1.      Obtain noncontrast head CT

2.      If CT is negative but suspicion for SAH remains, lumbar puncture is recommended in the AHA/ASA diagnostic pathway

3.      ACEP guidance allows LP or CTA in selected patients who remain at risk after a negative CT

4.      The choice between LP and CTA should consider the clinical context, test limitations, and shared decision-making

4.3 Lumbar Puncture

When indicated after a negative CT, CSF evaluation may demonstrate:

1.      Elevated red blood cells

2.      Xanthochromia

Findings must be interpreted in the context of a possible traumatic lumbar puncture.

LP is particularly important when presentation is delayed and clinical suspicion remains high despite negative CT imaging.

4.4 Vascular Imaging

Once SAH is identified, vascular imaging is required to determine the bleeding source.

1.      CTA is commonly obtained first to identify an intracranial aneurysm

2.      If CTA is negative or inconclusive and aneurysmal SAH remains suspected, digital subtraction angiography (DSA) is indicated

3.      In diffuse basal cistern or sylvian fissure SAH, DSA should be strongly pursued because small aneurysms or other vascular lesions may not be adequately identified on CTA

A diagnosis of aneurysmal SAH requires identification of an aneurysmal source, rather than CT evidence of subarachnoid blood alone.

5. Ottawa SAH Rule

In an appropriate alert patient with a new severe nontraumatic headache reaching maximal intensity within 1 hour, further investigation for SAH is indicated if any of the following are present:

1.      Age ≥40 years

2.      Neck pain or stiffness

3.      Witnessed loss of consciousness

4.      Onset during exertion

5.      Thunderclap headache

6.      Limited neck flexion on examination

The Ottawa SAH Rule is a screening rule, not a diagnostic test, and applies only to the population in which it was validated.

6. Other High-Yield Secondary Headaches

6.1 Meningitis

Fever + headache + meningismus ± altered mental status

Consider meningitis or encephalitis.

Evaluation may require:

1.      Blood cultures

2.      Neuroimaging when indicated

3.      Lumbar puncture

4.      Immediate empiric antimicrobial therapy when bacterial meningitis is suspected

6.2 Giant Cell Arteritis

Age ≥50 years + new headache + scalp tenderness + jaw claudication ± visual symptoms

Evaluate with:

1.      ESR

2.      CRP

3.      CBC

4.      Temporal and axillary artery imaging and/or temporal artery biopsy as appropriate

When suspicion is high, glucocorticoid treatment should not be delayed, particularly when visual symptoms are present.

6.3 Postpartum Headache

Postpartum headache with seizure, focal neurologic deficit, severe hypertension, or thunderclap onset should raise concern for:

1.      CVST

2.      PRES

3.      RCVS

4.      Preeclampsia or eclampsia

6.4 Raised Intracranial Pressure

Papilledema should prompt evaluation for raised intracranial pressure.

Papilledema with pulsatile tinnitus and transient visual obscurations may suggest idiopathic intracranial hypertension (IIH).

Evaluation generally includes:

1.      Brain imaging

2.      Venous imaging

3.      Lumbar puncture with opening pressure when it is safe to perform

6.5 Low CSF Pressure

Headache worse when upright and improved when supine suggests a low CSF pressure syndrome, including spontaneous intracranial hypotension.

6.6 Cervical Artery Dissection

Unilateral head or neck pain + partial Horner syndrome should raise concern for carotid artery dissection.

Urgent vascular imaging with CTA or MRA is appropriate.

6.7 Pituitary Apoplexy

Sudden severe headache + ophthalmoplegia ± visual loss

Consider pituitary apoplexy.

Urgent neuroimaging and endocrine assessment are required.

6.8 Acute Angle-Closure Glaucoma

Severe headache or ocular pain + painful red eye + halos + nausea/vomiting

Consider acute angle-closure glaucoma, an ophthalmic emergency.

7. Primary Headache Phenotypes

Primary headache should be diagnosed only after the clinical presentation has been assessed for concerning secondary causes.

7.1 Migraine Without Aura

Diagnostic features include ≥5 attacks lasting 4 to 72 hours.

At least 2 of the following:

1.      Unilateral location

2.      Pulsating quality

3.      Moderate or severe intensity

4.      Aggravated by or causing avoidance of routine physical activity

Plus at least 1 of:

1.      Nausea and/or vomiting

2.      Photophobia and phonophobia

A patient with a stable, typical migraine pattern and normal neurologic examination generally does not require routine neuroimaging.

7.2 Migraine With Aura

Typical aura symptoms are:

1.      Fully reversible

2.      Often positive phenomena

3.      Develop gradually

4.      May spread or occur sequentially

5.      Individual nonmotor aura symptoms typically last 5 to 60 minutes

6.      Motor aura may last up to 72 hours

Examples include:

1.      Scintillations or flashing lights

2.      Spreading paresthesias

3.      Reversible language symptoms

TIA more often produces sudden negative neurologic symptoms that are maximal at onset, although substantial clinical overlap exists.

7.3 Tension-Type Headache

Typical characteristics include:

1.      Bilateral location

2.      Pressing or tightening quality

3.      Mild to moderate intensity

4.      Not aggravated by routine physical activity

5.      Usually no nausea or vomiting

7.4 Cluster Headache

Typical cluster headache consists of:

1.      At least 5 attacks

2.      Severe or very severe unilateral orbital, supraorbital, or temporal pain

3.      Duration 15 to 180 minutes

4.      Attack frequency from one every other day to eight per day during active periods

5.      Ipsilateral autonomic features such as:

o    Lacrimation

o    Conjunctival injection

o    Nasal congestion or rhinorrhea

o    Eyelid edema

o    Ptosis or miosis

6.      Restlessness or agitation may occur

Acute treatment includes:

1.      High-flow 100% oxygen

2.      A rapid-acting triptan, such as subcutaneous or intranasal therapy, when appropriate

8. Imaging and Lumbar Puncture

8.1 Noncontrast Head CT

Particularly useful for:

1.      Acute intracranial hemorrhage

2.      SAH evaluation

3.      Trauma

4.      Major mass effect

8.2 MRI Brain

Useful when evaluating:

1.      Tumor

2.      Posterior fossa disease

3.      Demyelination

4.      Pituitary pathology

5.      Subtle or subacute intracranial abnormalities

8.3 CTV or MRV

Use when cerebral venous sinus thrombosis is suspected.

8.4 Lumbar Puncture

Important indications include:

1.      Meningitis or encephalitis

2.      Selected patients undergoing SAH evaluation

3.      Measurement of opening pressure

4.      Selected inflammatory or infectious neurologic disorders

When dangerous intracranial mass effect is suspected, assess the patient appropriately before performing LP.

9. Initial Management of Confirmed Aneurysmal SAH

Aneurysmal SAH is a neurologic emergency.

Initial priorities include:

1.      Airway, breathing, and circulation stabilization

2.      Immediate neurologic and neurosurgical or neurointerventional consultation

3.      Appropriate blood pressure monitoring and control, avoiding severe hypertension, hypotension, and large blood pressure variability

4.      Prompt identification and treatment of the ruptured aneurysm, preferably within 24 hours

5.      Endovascular coiling or surgical clipping depending on aneurysm and patient characteristics

6.      Early enteral nimodipine to reduce the risk of delayed cerebral ischemia and improve functional outcome

7.      Monitoring for:

o    Rebleeding

o    Hydrocephalus

o    Delayed cerebral ischemia and vasospasm

o    Seizures

o    Electrolyte and cardiopulmonary complications

10. Common Clinical Traps

1.      “Worst headache means migraine.”

o    A new thunderclap headache requires investigation for secondary causes

2.      “A normal CT excludes every dangerous headache.”

o    False. The diagnostic significance of CT depends on the suspected condition, timing, imaging quality, and clinical context

3.      “A normal neurologic examination excludes SAH.”

o    False

4.      “Papilledema is a feature of migraine.”

o    Papilledema indicates raised intracranial pressure until appropriately evaluated

5.      “Severe hypertension explains the headache.”

o    Evaluate for acute hypertensive target-organ injury and other secondary causes

6.      “Facial pressure means sinus headache.”

o    Migraine commonly produces facial pressure and sinonasal symptoms

11. Rapid Pattern Recognition

Thunderclap headache → SAH / RCVS / CVST / cervical artery dissection

Fever + meningismus → meningitis

Age ≥50 + jaw claudication → giant cell arteritis

Postpartum + seizure → eclampsia / PRES / CVST / RCVS

Papilledema → raised intracranial pressure

Orthostatic headache → low CSF pressure

Head or neck pain + Horner syndrome → carotid artery dissection

Sudden headache + ophthalmoplegia → pituitary apoplexy

Unilateral pulsating headache + nausea + photophobia/phonophobia → migraine

Bilateral pressing or tightening headache → tension-type headache

Severe orbital pain + tearing + restlessness → cluster headache

12. Key Clinical Insight

RED FLAGS FIRST.

A new thunderclap headache should be considered SAH until adequately excluded.

A normal neurologic examination does not exclude SAH.

In an appropriately selected neurologically intact patient, a normal high-quality noncontrast head CT performed within 6 hours can rule out nontraumatic SAH when imaging quality and interpretation are adequate.

At ≥6 hours, with a new neurologic deficit, or when clinical suspicion remains high despite negative CT imaging, further evaluation is required.

A change in headache pattern may be more clinically important than the absolute pain score.

References

1.      Hoh BL, Ko NU, Amin-Hanjani S, et al. 2023 Guideline for the Management of Patients With Aneurysmal Subarachnoid Hemorrhage: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2023;54(7):e314-e370. doi:10.1161/STR.0000000000000436.

2.      Godwin SA, Cherkas DS, Panagos PD, et al. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache. Ann Emerg Med. 2019;74(4):e41-e74. doi:10.1016/j.annemergmed.2019.07.009.

3.      Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1-211. doi:10.1177/0333102417738202.