Dr Reuben Streyer of EM Updates has created the following outstanding list of dangerous headaches on his post, Headaches in the Emergency Department: 13 Dangerous Headaches .
- Subarachnoid Hemorrhage
- Intracerebral Hemorrhage
- CNS Infection
- Increased Intracranial Pressure
- Carbon Monoxide Toxicity
- Acute Angle Closure Glaucoma
- Temporal (Giant Cell) Arteritis
- Cervical Artery Dissection
- Cerebral Venous Sinus Thrombosis
- Hypertensive Encephalopathy
- ENT/dental infection
- Idiopathic Intracranial Hypertension (Pseudotumor)
And here are Dr Strayer’s reminders on when to think of each cause [and after Dr. Strayer’s reminders, I have placed some of my thoughts and links to some resources inside brackets]:
emergency clinicians do not rule in migraine or other benign causes of headache. unless the headache is congruent to an established pattern for that patient, the history and physical specifically targets these 13 conditions.
subarachnoid hemorrhage: family history, PCKD, known berry aneurysm, sudden and maximal intensity at onset, posterior location [Key is, if you think of it, do a non-contrast head CT, and if CT is negative then do LP]
intracerebral hemorrhage: trauma, coagulopathy, decreased level of consciousness, hypertension [Key is, if you think of it, do non-contrast head CT. In May of this year the following was published: Guidelines for the Management of Spontaneous Intracerebral Hemorrhage [PubMed Abstract] [Full Text HTML] [Link To Download Full Text PDF]. Dr Mark Albert summarizes some of the new recommendations in a brief emedicine/medscape video of July 23, 2015.]
CNS infection: fever, immunocompromise, CNS instrumentation, recent head/face infection, meningismus [Key is, if CNS infection probable (possible?) promptly begin the indicated antimicrobial and/or antiviral. Don’t let the need for LP delay starting therapy. Also consider transfer to a neurointensivist who may consider beginning empiric therapy for an autoimmune encephalitis (as tests for this entity take a long time to come back)]
increased intracranial pressure: slowly progressive, cancer history, worse in morning, worse with head in dependent position, papilledema [See Etiology of Intracranial Hypertension for how to diagnosis–basically MRI is preferred but non-contrast head CT can be helpful initially (esp. if subarachnoid hemorrhage is suspected.]
Update 6-11-2018: See CritCases 8 Management of Elevated ICP, August 2017 from Emergency Medicine Cases. This awesome post has everything you need to know and do before the helicopter gets there.
carbon monoxide toxicity: contacts with similar illness, locationality (worse at home or at work) [See Carbon Monoxide Toxicity from emedicine/medscape updated Jan 27, 2015. See Workup for details on diagnosis (you must specifically order CO-oximetry as it is not included in a standard ABG)]
acute angle closure glaucoma: unilateral anterior location, precipitated by darkness, change in vision, red eye [See Acute Angle-Closure Glaucoma from emedicine/medscape updated Dec 2, 2014. See Workup.]
temporal (giant cell) arteritis: elderly, temporal location, jaw claudication, shoulder girdle symptoms [See Giant Cell Arteritis (Temporal Arteritis) from emedicine/meedscape updated Sept 25, 2014. “GCA should always be considered in the differential diagnosis of a new-onset headache in patients 50 years of age or older with an elevated erythrocyte sedimentation rate. Temporal artery biopsy remains the criterion standard for diagnosis of this granulomatous vasculitis.”]
cervical artery dissection: unilateral pain involving neck/face, trauma history [See outstaning article Focus On: Headache and Neck Pain–When to Suspect Cervical Artery Dissection from ACEP. “Once you suspect cervical artery dissection, choosing the appropriate imaging modality is the key. The usual approach to a new headache in the emergency department is a non-contrast head CT and possible lumbar puncture. Unfortunately, this may miss uncomplicated cervical artery dissection, leading to delays in the diagnosis and subsequent stroke or death.”. . . “The general consensus among experts is that CTA is the better screening test because it is faster, cheaper, and shows excellent visualization of large vessels, including the carotids and vertebrals. If CTA shows dissection, MRA is an appropriate follow-up test because it allows for better visualization of small vessels and will also show cerebral ischemia if present. A reasonable initial approach to a patient with a suspected cervical artery dissection would be to obtain a non-contrast head CT, and if negative, proceed with a CTA head and neck. If dissection is identified, obtain MR brain and MRA head and neck for further evaluation.”]
cerebral venous sinus thrombosis: thrombophilia, neurologic signs/symptoms in non-arterial distribution, eyelid edema, proptosis [What follows is from Cerebral Venous Thromosis, Circulation 2012:
Cerebral venous thrombosis, including thrombosis of cerebral veins and major dural sinuses, is an uncommon disorder in the general population. However, it has a higher frequency among patients younger than 40 years of age, patients with thrombophilia, and women who are pregnant or receiving hormonal contraceptive therapy. Annual incidence is estimated to be 3 to 4 cases per million.1 The incidence of cerebral venous thrombosis increases to 12 cases per 100 000 deliveries in pregnant women.2 Cerebral venous thrombosis occurs 3 times as frequently in women,3 likely because of increased risk during pregnancy and with hormonal contraceptive use.
The clinical presentation of cerebral venous thrombosis can be highly variable. Onset of symptoms and signs may be acute, subacute, or chronic. Four major syndromes have been described: isolated intracranial hypertension, focal neurological abnormalities, seizures, and encephalopathy. These syndromes may present in combination or isolation depending on the extent and location of cerebral venous thrombosis.
Intracranial hypertension resulting from cerebral venous thrombosis most frequently presents as headache. Headache is the presenting complaint in up to 90% of patients with cerebral venous thrombosis, and is described as subacute in onset 64% of the time.4,5
Focal neurological deficits are noted in 44% of patients with cerebral venous thrombosis.5 Motor weakness including hemiparesis is the most common focal finding, and may be present in up to 40% of patients.4 Fluent aphasia may result from left transverse sinus thrombosis. Sensory deficits are less frequent.
Focal or generalized seizures, including status epilepticus, are observed in 30% to 40% of patients with cerebral venous thrombosis.5,7Because seizures occur less often in other types of stroke, cerebral venous thrombosis should be considered in patients with seizures and other focal findings consistent with stroke. Seizures are encountered more frequently with thrombosis of the sagittal sinuses and cortical veins.7
Encephalopathy can result from thrombosis of the straight sinus and its branches or from severe cases of cerebral venous thrombosis with extensive cerebral edema, large venous infarcts, or parenchymal hemorrhages that lead to herniation.1 Elderly patients with cerebral venous thrombosis are more likely to present with mental status changes than younger patients.8
Head CT is the most frequently performed imaging study for evaluation of patients with new headache, focal neurological abnormalities, seizure, or change in mental status. Although noncontrast head CT may detect alternative diagnoses or demonstrate venous infarcts or hemorrhages, it has poor sensitivity and shows direct signs of cerebral venous thrombosis in only one third of patients.11
Magnetic resonance imaging of the head combined with MR venography is the most sensitive study for detection of cerebral venous thrombosis in the acute, subacute, and chronic phases.14
hypertensive encephalopathy: altered mentation, marked hypertension, improves with antihypertensive therapy [See Hypertensive Encephalopathy from emedicine/medscape April 14, 2015. What follows is from this article:
Hypertensive encephalopathy is a diagnosis of exclusion, and other potentially life-threatening causes must be considered in the assessment of a patient with neurologic deficits.
Malignant hypertension is associated with group 4 Keith-Wagener-Barker retinopathy, which is characterized by the presence of papilledema, heralding neurologic impairment from an elevated intracranial pressure (ICP)
With adequate control of hypertension, less than 1% of patients experience a hypertensive crisis. A hypertensive crisis is classified as either a hypertensive emergency or a hypertensive urgency, as follows:
A continuum exists between the clinical syndromes of hypertensive urgency and emergency; hence, the distinction between the 2 syndromes may not always be clear and precise in practice.
Hypertensive encephalopathy refers to the transient migratory neurologic symptoms that are associated with the malignant hypertensive state in a hypertensive emergency. The clinical symptoms are usually reversible with prompt initiation of therapy. In the evaluation of an encephalopathic patient, it is vital to exclude systemic disorders and various cerebrovascular events that may present with a similar constellation of clinical findings.
ENT/dental infection: ear, sinus, dental findings
idiopathic intracranial hypertension: young overweight female, hormone use, vision changes [See Etiology of Intracranial Hypertension for how to diagnosis–basically MRI is preferred but non-contrast head CT can be helpful initially (esp. if subarachnoid hemorrhage is suspected.]
preeclampsia: late pregnancy or postpartum