Headache (2024)

November 22, 2024November 22, 2024 ~ iEM Education Project Team ~ Leave a comment

by Shailaja Sampangi Ramaiah

You have a new patient!

A 60-year-old male is brought to the Emergency Room by a family who gives a history of sudden onset severe headache with vomiting and right-sided weakness. The symptoms began one hour ago. He is a known diabetic on Metformin and has been hypertensive on Losartan for the past 20 years. The patient has poor compliance with his home medications. The family denies any history of trauma, seizures, or antiplatelet or anticoagulation drug intake.

On examination, the patient is unresponsive with HR -98/min, BP: 210/120 mmHg, RR: 16/min, oxygen saturation: 80% room air, and temperature: afebrile. The GCS is 5 (E1V1M3), and the patient has right-sided weakness 0/5, absent deep tendon reflexes, glucose is 198mg/dl, and pupils are bilaterally midsized, equal, and reactive to light.

What do you need to know?

Headache is a common complaint in the Emergency Room (ER). It constitutes 1 – 4 % of all ER visits [1]. The true global prevalence of headache is unknown because the pathophysiology and causes of headache are broad. Headache disorders collectively constitute the seventh highest cause of years lived with disability (YLDS) [2].

Headaches are classified as primary headache disorders (when pain is the disease) and secondary headache disorders (when headache is a symptom of another disease). Primary headache disorders include migraine, tension headache, and cluster headache. Secondary headache disorders are listed below in Table 1.

Table 1 – Secondary headache disorders

Pathology	Examples
Headache attributed to head or neck trauma	Post-traumatic headache Concussion
Headache attributed to cervical or cranial vascular disorders	Subarachnoid hemorrhage Intraparenchymal hemorrhage Subdural or epidural hematoma Cavernous/venous sinus thrombosis Arteriovenous malformation Temporal arteritis Carotid/vertebral artery dissection
CNS infections	Meningitis Encephalitis Cerebral abscess
Intracranial non vascular space occupying lesions	Tumors Parasitic or inflammatory lesions
Headache attributed to substance or withdrawal	Nitrates and nitrites Mono amine oxidase inhibitors Alcohol withdrawal Abuse of analgesics
Headache or facial pain due to head, ears, eyes, nose, or throat disorders	Glaucoma Sinusitis Optic neuritis Iritis
Headache attributed to altered homeostasis	Fasting headache High altitude cerebral edema Hypoxia Hypercarbia Hypothyroidism Obstructive sleep apnea
Miscellaneous causes	Preeclampsia Post dural puncture headache

Most patients presenting to the ER with headache have a primary headache disorder, with migraine being the most common [3]. However, it is vital to evaluate for headache signs and symptoms that point towards secondary causes. The SNNOOP 10 list in Table 2 reviews important red flag signs and symptoms to consider in a patient with headache [4].

Table 2 – Red flag signs and symptoms of headache (SNNOOP 10 list)

Sign or symptom	Related secondary headache cause
Systemic symptoms including fever	Headache attributed to infection or nonvascular intracranial disorders, like carcinoid or pheochromocytoma
Neoplasm in history	Neoplasms of the brain, metastasis
Neurologic deficit or dysfunction (including decreased consciousness)	Headaches attributed to vascular, nonvascular intracranial disorders; brain abscess and other infections
Onset of headache is sudden or abrupt	Subarachnoid hemorrhage and other headaches attributed to cranial or cervical vascular disorders
Older age (after 50 years)	Giant cell arteritis and other headache attributed to cranial or cervical vascular disorders; neoplasms and other nonvascular intracranial disorders
Pattern change or recent onset of headache	Neoplasms, headaches attributed to vascular, nonvascular intracranial disorders
Positional headache	Intracranial hypertension or hypotension
Precipitated by sneezing, coughing, or exercise	Posterior fossa malformations; Chiari malformation
Papilledema	Neoplasms and other nonvascular intracranial disorders; intracranial hypertension
Progressive headache and atypical presentations	Neoplasms and other nonvascular intracranial disorders
Pregnancy or postpartum	Headaches attributed to cranial or cervical vascular disorders; post dural puncture headache; hypertension-related disorders (e.g., preeclampsia); cerebral sinus thrombosis; hypothyroidism; anemia; diabetes
Painful eye with autonomic features	Pathology in posterior fossa, pituitary region, or cavernous sinus; Tolosa-Hunt syndrome; ophthalmic causes
Posttraumatic onset of headache	Acute and chronic posttraumatic headache; subdural hematoma and other headache attributed to vascular disorders
Pathology of the immune system such as HIV	Opportunistic infections
Painkiller overuse or new drug at onset of headache	Medication overuse headache; drug incompatibility

Primary Headache Disorders

Migraine

Migraines are one of the most common primary headache disorders. Migraines affect females more than males and are more common in the third and fourth decade of life. The clinical presentation includes unilateral or bilateral pulsating pains with moderate to severe intensity. Migraines may have associated auras, photophobia, phonophobia, blurred vision, lightheadedness, vertigo, nausea, and vomiting. Most patients seek dark, quiet rooms. The triggers for migraines include sleep deprivation, hunger, hormonal changes during menstruation, and certain medications (e.g., nitrates and oral contraceptive pills) [5].

Cluster Headache

Cluster headaches occur suddenly, last 15 minutes to 3 hours in duration, and tend to occur repeatedly during a defined time interval. This type of headache is more common in men than women. Precipitating factors include ingestion of alcohol, stress, and climate change. The headache begins as unilateral sharp stabbing pain in the eye, exclusively in the trigeminal territory, accompanied by ipsilateral autonomic symptoms such as ptosis, miosis, forehead, and facial swelling [5].

Tension Headache

Tension headaches, like migraines, are a common cause of primary headaches and affect women more than men. Tension headaches may last from minutes to days. Physical examination reveals tender areas on the scalp and neck. Patients complain of a tight, band-like discomfort around the head that is non pulsating and dull in nature. The headache does not worsen with physical activity. Anxiety and depression may coexist with chronic tension type headaches [6].

Secondary Headache Disorders

There are various secondary causes of headaches, ranging from benign to severe. This section will focus on a small list of etiologies relevant to the emergency medicine practitioner.

Subarachnoid Hemorrhage (SAH)

SAH is a life-threatening cause of headache that should be considered in all ER patients with headache. Accumulation of blood in the subarachnoid space activates meningeal nociceptors, causing headache and meningismus. Causes for non-traumatic SAH include ruptured saccular aneurysms, arteriovenous malformations, cavernous angiomas, and coagulopathy. The risk of brain aneurysmal rupture increases with age, hypertension, smoking, excessive alcohol consumption, and use of sympathomimetic drugs [7].

Patients with SAH historically present with a severe, acute onset headache that is maximal intensity at onset (thunderclap headache). The onset of headache may be spontaneous or after physical exertion. Associated signs and symptoms are nausea, vomiting, neck stiffness, photophobia, seizures, depressed consciousness, and focal neurological abnormalities. Retinal hemorrhage may be present on fundoscopic examination. SAH patient prognosis can be predicted with the Hunt and Hess classification system [7], as shown in Table 3.

Table 3 – Hunt and Hess classification of cerebral aneurysms and subarachnoid hemorrhage

Grade	Condition
0	Unruptured aneurysm
1	Asymptomatic or minimal headache and slight nuchal rigidity
2	Moderate or severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy
3	Drowsiness, confusion or mild focal deficit
4	Stupor, moderate to severe hemiparesis
5	Deep coma, decerebrate posturing, moribund appearance

Grades 1 or 2 – good prognosis
Grade 3 – moderate prognosis
Grades 4 or 5 – poor prognosis

Intracranial Neoplasms

Headache is a common presenting symptom of patients with a brain tumor, but the symptoms are variable. Symptoms depend on the site of tumor, traction on meninges or large vessels, increase in intracranial pressure, or hydrocephalus. Other than headache, patients may have sleep disturbances, nausea and vomiting, seizures, focal neurologic deficits, alterations in consciousness, personality disorders, and cognitive difficulties [8].

Meningitis

Acute bacterial meningitis may present with headache, fever, nuchal rigidity, nausea, vomiting, photophobia, new skin rash, seizures, focal neurologic deficits, or alterations in consciousness. The most common pathogens causing bacterial meningitis in adults are Streptococcus pneumoniae and Neisseria meningitidis. Bacterial meningeal invasion occurs when bacteria colonize host mucosal epithelium, invade and survive within the bloodstream, cross the blood-brain barrier, and multiply within the CSF. Once inflammation is initiated, a series of injuries occur to the endothelium of the blood-brain barrier that result in vasogenic brain edema, loss of cerebrovascular autoregulation, and increased intracranial pressure. This results in localized areas of brain ischemia, cytotoxic injury, and neuronal death [9].

Giant Cell Arteritis (GCA, or Temporal arteritis)

GCA is an inflammatory vasculopathy affecting mainly the extracranial branches of the carotid artery (temporal and occipital). The common features of giant cell arteritis are advanced age, female gender, headache, visual symptoms, jaw claudication, temporal artery tenderness, and systemic symptoms (e.g., fever, weight loss, fatigue). One of the most serious complications of GCA is blindness, but a range of visual symptoms and signs may occur, such as diplopia, visual field deficits, amaurosis fugax, or an afferent pupillary defect. Typical GCA headaches are worse in the morning than later in the day and can be constant or intermittent. Other complications include transient ischemic attacks, peripheral neuropathies, and stroke. Palpation of the temporal artery may reveal absent pulses, erythema, and nodular swellings [10].

Carotid and Vertebral Artery Dissection

The classic symptoms of carotid artery dissection include:

Unilateral headache or neck pain.
Ipsilateral partial Horner’s syndrome.
Blindness (dissection into retinal artery).
Contralateral motor deficits.

Vertebral artery dissection may also present with severe unilateral headache or neck pain. Dissection along the vertebral artery may result in brainstem or cerebellar ischemia, causing vertigo, vomiting, diplopia, ataxia, tinnitus, unilateral facial weakness, alterations in consciousness, or cranial nerve deficits.

Both carotid and vertebral artery dissection should be considered in a patient presenting with headache or neck pain with a history of recent head or neck trauma, sudden neck movement, neck torsion, coughing, chiropractic manipulation, minor falls, weight lifting, basketball, volleyball, or a motor vehicle collision [11].

Cerebral Vein Thrombosis (CVT)

Patients with this diagnosis often have a headache lasting days to weeks, along with other signs and symptoms, like seizures, focal neurologic deficits, orbital pain, proptosis, chemosis, and papilledema. Symptoms are due to raised intracranial pressure from occlusion of the cerebral venous system, causing ischemia, infarction, or hemorrhage.

Major risk factors for CVT include pregnancy, post-partum state, malignancy, head trauma, recent surgery, parameningeal infections, oral contraceptives, history of vasculitis, inflammatory bowel disease, and connective tissue disease [12].

Initial Assessment and Stabilization (ABCDE approach)

When a patient presents with headache to the ER, it is vital to follow the ABCDE sequence of initial assessment.

Airway: look for airway patency. Assess if the patient is talking normally or if there are signs of airway obstruction or aspiration. Patients with SAH, intraparenchymal bleed, CVT, or recent seizure may have airway compromise due to poor GCS. These patients may require interventions, such as manual opening of the airway with a head-tilt-chin lift or jaw thrust maneuver, insertion of an oropharyngeal or nasopharyngeal airway, or suctioning of secretions or vomitus from the airway. Patients with GCS under 8 should be considered for supraglottic airway insertion or endotracheal intubation.
Breathing: look for tachypnea or bradypnea, changes to oxygen saturation, and abnormal breath sounds. Intracranial bleeds or mass lesions may influence the central respiratory center, causing decreased, abnormal, or absent respirations [7]. Administer supplemental oxygen for hypoxia. Consider oxygen via face mask, positive pressure bag valve mask ventilation, or intubation, based on respiratory effort, GCS, and concern for aspiration.
Circulation: check the heart rate, blood pressure, peripheral and central pulses, and capillary refill time. Severe hypertension with headache and altered mentation should raise concern for intracranial bleeding [7]. Headache with severe hypertension in a pregnant patient should raise concern for pre-eclampsia or eclampsia. Fever with headache should raise concern for infectious conditions, like meningitis or encephalitis. Intravenous antihypertensive medications should be initiated during this step if needed. Monitor for bradycardia, hypertension, and abnormal breathing, which can indicate impending brain herniation from elevated intracranial pressure.
Disability: check pupillary size and reactivity, calculate a Glasgow coma score, and check a glucose level. Perform a focused neurological examination with assessment of the cranial nerves, sensory and motor function, and cerebellar signs. Patients with complex migraine headaches may exhibit photophobia, diplopia, paresthesias, dysarthria, tinnitus, or vertigo. Patients with stroke, intraparenchymal bleeding, subarachnoid hemorrhage, CVT, carotid or vertebral artery dissection, intracranial space-occupying lesions, and encephalitis may present with focal neurological deficits and varying levels of GCS [7,8].
Exposure: Fully undress your patient and perform a head-to-toe examination. Any signs of head trauma, including headache, should raise suspicion for intracranial bleeding. Petechiae and purpura on the skin may point towards infective pathologies, like septicemia or meningococcal meningitis [13].

Medical History

A detailed history in a patient with headaches can provide clues to the cause. Ask your patient about the time of symptom onset, pain location, headache characteristics, and associated symptoms. Ask about past medical history, surgical history, relevant family history, and drug or alcohol use.

Time of onset: sudden onset symptoms may be seen in subarachnoid hemorrhage, ischemic or hemorrhagic strokes, or carotid artery dissection. Gradual onset of symptoms is more common in migraine, cluster headache, tension headache, headaches due to infective pathology, and CVT [5,6].
Site of headache: Most migraine and cluster headaches present with unilateral pain with cluster headache involving branches of the trigeminal nerve (around orbit). Tension headaches present more often as bilateral head pain. Sinus headaches have pain behind the maxillary and frontal sinuses [5,6].
Characteristics and associated symptoms: Migraines are associated with auras, photophobia, phonophobia, blurred vision, lightheadedness, nausea, or vomiting [5]. Cluster headaches may have ipsilateral autonomic symptoms, such as ptosis, miosis, eye tearing, or facial swelling [5]. Tension headaches may present with tender areas on the scalp and neck [6]. Ask about associated symptoms for secondary headaches, like fever and neck stiffness (meningitis), vision changes (acute glaucoma, giant cell arteritis), new seizures, vomiting, or focal motor or sensory changes (space-occupying lesion, intracranial bleeding, CVT, etc.) [8-10,12].
Risk factors:
- Intraparenchymal Bleeding: hypertension, smoking, alcohol abuse, anticoagulation medication usage, recent head trauma [3,7].
- Subarachnoid Bleeding: hypertension, smoking, cocaine use, family history of brain aneurysms in close relatives, polycystic kidney disease, Marfan syndrome, Ehlers-Danlos syndrome [7].
- Carotid Artery Dissection: recent neck trauma, recent neck torsion during sporting activities or medical treatments (e.g., chiropractic maneuvers) [11]
- Cerebral Venous Thrombosis: pregnancy, recently postpartum, oral contraceptive use, hypercoagulable conditions (thrombophilias, antithrombin III, protein C and S deficiency, factor V Leiden mutation, antiphospholipid syndrome, malignancy), recent surgery [12].
- Post Dural Puncture Headache: recent lumbar puncture

Physical Examination

Patients presenting with headache should undergo a thorough head-to-toe physical exam after the ABCDE assessment. Special care should be taken in examining the head, ears, eyes, neck, and throat, as well as in performing a focused neurological exam. The neurological exam should include calculating a Glasgow coma score, cranial nerve testing, assessment of motor and sensory deficits in the extremities, and assessment of gait and coordination. A full set of vitals, including a temperature and glucose level, should be taken.

When To Ask Your Senior for Help

If you are immediately concerned about a life-threatening condition, or if the patient needs any interventions during the ABCDE assessment, you should notify a supervising doctor.

Patient details that should trigger you to alert your senior:

Inability to talk or
Altered breathing pattern or use of accessory muscles of respiration
Severe hypertension, hypotension, or hypoxia
Asymmetric pupillary sizes
Severe headache with acute onset
Signs of meningeal irritation or raised intracranial pressure

Not-To-Miss Diagnoses

Headaches have many causes. As an emergency medicine provider, it is important not to miss certain diagnoses that have a high rate of morbidity or mortality. Some diagnoses to always consider in the patient with headache are intraparenchymal bleeding, subarachnoid bleeding, giant cell arteritis, acute glaucoma, meningitis, encephalitis, cerebral vein thrombosis, carotid and vertebral artery dissection, brain malignancy, and pre-eclampsia.

Acing Diagnostic Testing

The investigations you order for your headache patient will depend on your history, physical exam, and top conditions on your differential diagnosis list.

Some investigations to consider in headache patients:

Glucose testing should be ordered in any patient with headache plus altered mental status, focal neurologic deficits, or seizures.
Urine pregnancy testing should be ordered for any female of child-bearing age presenting with headache.
ECG abnormalities in the form of arrhythmias and non-specific ST-T wave changes can be seen in patients with intracranial bleeding or space-occupying lesions
Complete blood count can help support infective etiologies if leukocytosis is present.
Serum chemistry is used to evaluate for any electrolyte abnormalities in patients with new seizures or vomiting.
ESR or CRP is considered if you are concerned about Giant cell arteritis [10]
HIV testing is considered based on the history and physical exam if there are clinical signs of immunocompromise
CT or MRI imaging is often unnecessary in a patient with a primary headache. It should be ordered based on patient history and physical exam, particularly with concerns for SAH, intracranial bleeding, or a space-occupying lesion should have non-contrast CT brain imaging [7,8]. Patients with concerns for carotid or vertebral artery dissection should have a CT angiogram of the neck and head [11]. Patients with concerns for cerebral venous thrombosis should have an MR venogram or CT venogram [12].

Examples of CT images of patients with conditions that may present with headache are below.

Figure 1a (left) and Figure 1b (right): Subarachnoid bleed on CT brain without contrast. Acute bleeding is demonstrated as a bright white (radio-opaque) substance. The distribution of blood seen in Figure 1a is sometimes termed the “starfish of death.”

Empiric and Symptomatic Treatment

Medications for symptom control should be considered for any patient with headache and other associated symptoms. Table 4 below lists some common medications to consider for migraine headaches.

Table 4- Medications for migraine headaches

Drug	Dose	Comments
Acetaminophen	500 – 1000 mg PO every 6hrs	Safe in pregnancy
Ibuprofen	600 -800 mg PO every 6hrs	Can cause GI upset Avoid in pregnancy Caution in patients with renal insufficiency
Ketorolac	15-30 mg IV or IM every 6hrs	Same as ibuprofen
Metoclopramide	10 mg IV or IM every 6hrs	Administer slowly to avoid extrapyramidal symptoms
Diphenhydramine	25-50 mg IV or IM every 6hrs	May cause drowsiness
Dihydroergotamine	1 mg IV or IM Maximum 3mg/24hours	Contraindicated in pregnancy, uncontrolled HTN, or coronary artery disease
Sumatriptan	6 mg SC injection x 1 (max 12mg SC/24hrs)	Same as Dihydroergotamine

Basic analgesics, like acetaminophen or NSAIDs, are first-line treatments for tension headaches [6]. High-flow oxygen therapy via a non-rebreather mask at 12-15 liters/min is the first-line treatment for cluster headaches [5].

Patients with signs and symptoms of elevated intracranial pressure (e.g., asymmetric pupil size, depressed GCS, vomiting, etc.), brain edema on CT imaging, or impending herniation on CT imaging should receive IV mannitol, IV 3% NaCl, or IV steroids, in consultation with a neurosurgical specialist [8]. High-dose IV steroids are also used in patients with giant cell arteritis [10].

There is no role for routine prophylactic antiepileptic medications in patients with headache and most types of intracranial bleeding. However, antiepileptics, like Levetiracetam, are generally well tolerated and are sometimes recommended by neurosurgical specialists for seizure prevention. For most patients with headache and seizure, IV benzodiazepines should be first-line for seizure treatment. One exception is eclampsia, where IV magnesium is the preferred therapy.

Anticoagulation, such as IV unfractionated heparin, should be administered in patients with cerebral venous thrombosis and for extracranial carotid or vertebral artery dissection [11]. Patients presenting with headache and signs of ischemic stroke may be candidates for thrombolysis with IV Alteplase or Tenecteplase, depending on local resources and the time since symptom onset. IV antibiotics should be administered empirically for patients with headache with suspected meningitis or encephalitis [3,9].

Procedures

Lumbar Puncture [14]

Indications for the procedure: CSF collection with a lumbar puncture can help to evaluate for a CNS infection, such as meningitis. This procedure can also assist in assessing for subarachnoid hemorrhage. CT head is highly sensitive in detecting SAH in the first 6 hours after headache onset, but the sensitivity diminishes beyond hour 6. A lumbar puncture can be considered in a patient with deep clinical concern for SAH and a negative CT scan with symptoms over 6 hours [7].
Contraindications: Raised intracranial pressure (e.g., brain mass or intracranial bleeding with midline shift on CT), coagulopathy, or trauma or infection at the site of needle insertion
Complications: Bleeding, infection, post-dural puncture headache, pain during the procedure

Before the procedure:

Explain the procedure, obtain consent, and gather materials (Figure 6) to maintain aseptic precautions.
Place the patient in the lateral decubitus or seated position.
Identify the highest points of iliac crests bilaterally.

The equipment needed for a lumbar puncture procedure includes a sterile lumbar puncture tray, which typically contains a spinal needle with stylet (commonly 20G–22G), local anesthetic (e.g., lidocaine), antiseptic solution (e.g., povidone-iodine or chlorhexidine), sterile gloves, drapes, and gauze. Additionally, a manometer with tubing is required for measuring cerebrospinal fluid (CSF) pressure, along with collection tubes for CSF sampling. Optional items may include a face mask, eye protection, and an assistant for patient positioning and monitoring.

To identify the L4 interspace for a lumbar puncture (Figure 7), start by positioning the patient appropriately—either sitting and leaning forward or lying in the lateral decubitus position with knees drawn to the chest and the back flexed to maximize exposure of the vertebral spaces. Palpate the iliac crests on both sides, noting their highest points. Draw an imaginary line connecting these points, known as the intercristal or Tuffier’s line, which usually crosses the spinous process of the L4 vertebra. The L4-L5 interspace is located just below this line. Confirm the space by palpating the spinous processes to ensure accurate identification before proceeding.

This level corresponds to L4-L5 intervertebral space where the spinal needle should be inserted. Instruct the patient to arch their spine posteriorly to open the interspinous spaces. Clean and drape the area. Administer local anesthesia to the planned site of the procedure. Prepare four marked containers to collect the CSF. Using aseptic technique, advance the spinal needle at the L4-L5 interspace until a popping sensation is felt and CSF drips from the spinal needle. Measure CSF opening pressure by connecting a manometer as soon as fluid appears and note the reading. Collect about 1 mL of CSF in all 4 marked containers in a consecutive fashion (Figure 8). Once sufficient CSF is collected, place the stylet back in the needle, remove the spinal needle, and cover the site with gauze or a Band-Aid. Send the CSF to the laboratory for analysis, re-evaluate your patient, and provide advice regarding puncture headache [14].

The chart below describes how CSF is interpreted by the clinician once it is analyzed by the laboratory.

Table 5 – CSF interpretation [15]

	Normal	Bacterial Meningitis	Viral Meningitis	Subarachnoid Hemorrhage
Opening pressure (mmHg)	7-18	>30	Normal	Increased
Appearance	Clear, colorless	Turbid	Clear	Xanthochromia present
Protein (mg/dl)	23-38	Increased	Normal to decreased	Increased
Glucose	2/3^rd of serum glucose	Decreased	Normal	Normal
Gram stain	Negative	Positive	Negative	Negative
WBC count	<5 cells	Predominantly neutrophils	Predominantly lymphocytes	May be increased due to bleeding

Special Patient Groups

Pregnant Patients

Pregnant patients with headache are at increased risk for some diagnoses more than nonpregnant women due to pregnancy being a hypercoagulable state. Pregnant patients with headaches are unable to receive all the same medications as nonpregnant patients. Headache medications that are safe in pregnancy are paracetamol, metoclopramide, diphenhydramine, magnesium, and opioids for severe pain. Drugs to avoid during pregnancy include ergotamine, NSAIDS, valproate, lithium, and topiramate [16]. Specific causes of headache to consider in pregnancy are pre-eclampsia, eclampsia, cerebral venous thrombosis, and stroke. Treatment of headache should primarily focus on the cause [16].

Children

Headache is a common cause of ED visits in the pediatric population [17]. The causes of headaches in the pediatric population range from more benign primary headache etiologies to more secondary severe etiologies. CT imaging should be limited to cases where more serious signs and symptoms are present, such as change in behavior, confusion, unexplained vomiting, unexplained high fevers, head trauma, or focal neurologic deficits [17]. Medications for pediatric headaches are weight-based in their dosing. The standard pediatric dose for ibuprofen is 10 mg per kilogram (mg/kg) of body weight per dose. This dosage can be administered every 6 to 8 hours as needed, with a maximum of three doses in a 24-hour period. It’s important not to exceed a total daily dose of 40 mg/kg or 1,200 mg, whichever is less. For acetaminophen, the recommended pediatric dose ranges from 10 to 15 mg/kg per dose. This can be given every 4 to 6 hours as needed, with a maximum of five doses in 24 hours. The total daily dose should not exceed 75 mg/kg or 3,000 mg, whichever is less.

Elderly

Elderly patients experiencing headaches may have additional health conditions that raise the risk of serious underlying causes, such as a history of hypertension, cancer, previous brain surgeries, stroke, or the use of anticoagulant medications. When evaluating and treating these patients, it’s important to tailor your approach based on the suspected diagnosis. However, it is advisable to have a lower threshold for ordering diagnostic tests in elderly patients with unexplained headaches.

When To Admit

Primary headache disorders, like migraine, cluster headache and tension headaches, do not require admission and should be treated symptomatically in the ER. Upon discharge, these patients should be advised to have adequate sleep, stay hydrated, consume regular meals, and avoid any headache triggers. Patients with a headache secondary to a dangerous etiology, such as meningitis or intracranial bleeding, should be admitted for further treatment and monitoring. Patients with red flag signs or symptoms of a dangerous etiology should also be admitted for further management, even without a confirmed diagnosis.

Revisiting Our Patient

You return to your 60-year-old male patient with sudden onset headache and right-sided weakness. You note his severe hypertension, hypoxemia, right-sided motor deficits, and low GCS.

You follow your ABCDE approach to be sure not to miss any critical steps in management.

Airway: This patient has a depressed mental status and no gag reflex. You notice some secretions in his airway and prepare for intubation.
Breathing: His lungs are bilaterally clear and equal. After his airway is suctioned, you apply supplemental oxygen via a non-rebreather mask.

After the patient is intubated, you continue your assessment.

Circulation: The patient continues to be hypertensive to 210/120 mmHg after intubation. You administer IV labetalol 10mg and begin a fentanyl infusion for sedation.
Disability: The glucose is 198mg/dL. Your initial brief exam demonstrated right-sided motor deficits and normal mid-sized pupils.
Exposure: There are no physical signs of trauma or rashes on the exam

Once the patient is stabilized, he receives a CT head without contrast, showing an acute subarachnoid bleed. Basic pre-operative laboratory tests are drawn and you contact the neurosurgeon on call. The neurosurgery team recommends strict blood pressure control and admission to the ICU for operative management. You explain the diagnosis and plan of care to the patient’s family with understanding and agreement.

Author

Shailaja Sampangi Ramaiah

Dr. Shailaja Sampangi Ramaiah is a Professor and Head of Emergency Medicine at Father Muller Medical College, Mangalore, India. With advanced qualifications in anesthesia and medical education, she is a FAIMER fellow and ACME-certified educator. Dr. Shailaja leads initiatives in simulation training and clinical quality improvement and is a life member of several prestigious medical associations. She is passionate about advancing emergency care education.

Listen to the chapter

References

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Reviewed and Edited By

Joseph Ciano, DO, MPH, MS

Dr. Ciano is a board-certified attending emergency medicine physician from New York, USA. He works in the Department of Emergency Medicine and Global Health at the Hospital of the University of Pennsylvania. Dr. Ciano’s global work focuses on capacity building and medical education and training in low-middle income countries. He is thrilled to collaborate with the iEM Education Project in creating free educational content for medical trainees and physicians.

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Meningitis (2024)

November 13, 2024November 13, 2024 ~ iEM Education Project Team ~ Leave a comment

by J. Austin Lee

You have a new patient!

A 21-year-old male presented to a clinic. He is a refugee and has been here with a high-grade fever and a severe headache for the past three days. The patient had been working as a laborer in construction sites in the area for the past six months. At triage, his vital signs are as follows: temperature of 39.1°C (102.5°F), blood pressure of 110/70 mmHg, heart rate of 110 beats per minute, and respiratory rate of 22 breaths per minute.

Further examination reveals that the patient is quite photophobic. You note that he prefers to sit still, and when you examine him further, you feel that his neck is quite uncomfortable when flexed, and there is discomfort with flexed hips and passive knee extension. The patient was accompanied by a co-worker who reported that this morning, the patient was vomiting and had been confused. The patient had no history of recent travel or vaccination.

What do you need to know?

Importance

Meningitis is an important infectious disease with severe consequences if not promptly recognized and treated. Meningitis is caused by inflammation of the meninges, the membranes covering the brain and spinal cord. It can be caused by a bacterial, viral, fungal, or parasitic infection. Moreover, meningitis can be triggered by physical injury, autoimmune disorders, cancer, or certain drugs that can cause meningitis. Generally, when discussing meningitis, we are primarily concerned with infectious etiologies. In addition to the high mortality associated with meningitis, survivors may suffer from long-term sequelae, such as hearing loss, cognitive impairment, and neurologic deficits [1]. Infants, children, and immunocompromised patients are at a higher risk of developing meningitis, and outbreaks can occur in crowded living conditions, with classic examples including crowded urban areas (including slums), university dormitories, and military barracks [2]. Prompt recognition and treatment with appropriate antibiotics or antivirals are critical for improving outcomes in patients with meningitis [3].

Epidemiology

Meningitis is a significant global health problem, particularly in low- and middle-income countries. According to the World Health Organization (WHO), there are an estimated 1.2 million cases of bacterial meningitis each year, resulting in 250,000 deaths [4]. According to the Global Burden of Disease study, meningitis is responsible for an estimated 21.9 million disability-adjusted life years (DALYs) globally [5]. The burden of meningitis is particularly high in sub-Saharan Africa, where large-scale epidemics of meningococcal meningitis occur. In these regions, outbreaks are often associated with overcrowding, malnutrition, and poor sanitation, and can cause high rates of mortality and long-term disability. While vaccination has helped to reduce the burden of meningitis in many parts of the world, there is still a need for continued surveillance and control measures, particularly in high-risk populations.

Pathophysiology

Bacteria (and viruses and chemicals) can cross the blood-brain barrier to infect or inflame the meninges by spreading from the bloodstream. Pathogens can also spread from contiguous infection (from a source such as the sinuses or middle ear), trauma, neurosurgery, or indwelling medical devices [6]. Nasopharyngeal colonization from infected droplets of respiratory secretions or distant localized infection (lungs, urine) with subsequent bloodstream invasion are other sources of infection [6].

Once the pathogen reaches the meninges, it triggers an immune response, releasing pro-inflammatory cytokines, which attract immune cells to the site of infection. This immune response leads to the characteristic symptoms of meningitis, including fever, headache, neck stiffness, and altered mental status. In severe cases, the inflammation can lead to increased intracranial pressure, cerebral edema, and brain herniation, which is life-threatening and frequently fatal [6].

Bacterial meningitis poses an emergent risk to the neurological system; progression can result in rapid fatality. Furthermore, bacterial meningitis has the potential to cause long-term complications, including hearing and vision impairment, memory and concentration issues, epilepsy, coordination and balance difficulties, learning challenges, and behavioral disorders [6]. In community-acquired meningitis, S. pneumoniae has become the most common pathogen since routine immunization of infants against H. influenzae type B [7]. It’s important to note that the most common causes of meningitis can vary depending on the patient’s age, geography, and immune status [8]. Table 1 summarizes most common pathogens of meningitis.

Table 1: Common Infectious Causes of Meningitis [7-14].

Pathogen	Common Etiologies
Bacteria	Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae, Listeria monocytogenes
Viruses	Enteroviruses (e.g. Coxsackie virus, Echovirus), Herpes simplex virus, Varicella-zoster virus, Mumps virus
Fungi	Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis
Parasites	Naegleria fowleri, Acanthamoeba species

Medical History

Key features in the medical history of meningitis include the onset and duration of symptoms, recent travel or exposure to infectious agents, immunization status, underlying medical conditions, and medication use. It is important to obtain a detailed history of present illness, including the timing and progression of symptoms such as fever, headache, neck stiffness, altered mental status, and rash. Patients may also report symptoms such as nausea, vomiting, photophobia, and seizures. Recent travel or exposure to individuals with known or suspected meningitis can help identify potential infectious agents. Immunization status, particularly regarding vaccines against meningococcal and pneumococcal infections, is also important to determine. Patients with chronic medical conditions or who are taking immunosuppressive medications may be at increased risk for certain pathogens or complications.

Physical Examination

The physical exam findings in a patient with meningitis include vital signs, general appearance, and specific neurological findings. Vital signs such as fever, tachycardia, and hypotension are common. Patients may appear acutely ill, with a lethargic or altered mental status. They may exhibit signs of meningeal irritation, such as photophobia, neck stiffness, and a positive Kernig or Brudzinski sign. Kernig’s sign is the inability to straighten the leg when the hip is flexed to 90 degrees; Brudzinski’s sign is positive when forced flexion of the neck elicits a reflex flexion of the hips [6]. Both Kernig and Brudzinski have reported low sensitivity (5%) but high specificity (95%) [6]. Neurological findings such as altered level of consciousness, focal neurologic deficits, and seizures may also occur or be present. Skin findings such as a petechial or purpuric rash may present in meningococcal meningitis patients. In infants, bulging fontanelles and poor feeding are concerning. Jolt accentuation testing can provide additional value: the patient horizontally rotates the head at two to three rotations per second [15]. The worsening of an existing headache indicates a positive result, though the sensitivity of jolt accentuation for diagnosing meningitis varies widely, with estimates ranging from 40-96% [15].

Table 2: Common signs/symptoms of meningitis, with sensitivity [8-10]

Sign / Symptom	Sensitivity
Neck stiffness	30-100
Headache	70-100
Photophobia	50-90
Nausea/vomiting	50-90
Altered mental status	50-80
Jolt accentuation	40-90
Fever	70-80
Seizures	10-30
Focal neurological deficits	<10

Alternative & Differential Diagnoses

Encephalitis: inflammation and swelling of the brain parenchyma; encephalitis tends to cause more neurological symptoms such as confusion, seizures, and changes in behavior or personality.
Chemical meningitis (e.g., due to contrast agents, medications, or illicit drugs): The patient should have a history of exposure to a triggering agent, such as a medication or contrast dye.
Carcinomatous meningitis (e.g., metastatic cancer cells in cerebrospinal fluid); history or imaging with evidence of metastatic disease.
Aseptic meningitis (e.g., due to autoimmune disorders, sarcoidosis, or drug reactions) symptoms are usually milder. They may include fever, headache, and neck stiffness, often including other symptoms such as rash or joint pain.
Cerebral vasculitis is inflammation and damage to the blood vessels that supply the brain. It may have a more insidious onset and a chronic or recurrent course.
Traumatic meningitis (e.g., due to head injury or neurosurgical procedures)
Brain abscess or subdural empyema; likely to include more focal neurological symptoms/deficits such as weakness or paralysis, seizures, or speech and vision problems.
Subarachnoid bleeding is commonly associated with sudden, severe headaches, nausea, vomiting, and, at times, syncope.
Tetanus is commonly associated with other symptoms such as jaw stiffness, diffuse muscle rigidity/spasm, difficulty swallowing, and respiratory distress.
Malaria, particularly cerebral malaria, is typically found in areas with high transmission rates of malaria, and cerebral malaria typically has a more gradual onset. It can progress over several days to weeks.

Acing Diagnostic Testing

Acute diagnostic testing is crucial in managing meningitis as it allows for early detection and appropriate treatment. The accepted gold standard for diagnosing meningitis is cerebrospinal fluid (CSF) analysis, obtained through a lumbar puncture [6,16]. CSF analysis includes cell count, protein and glucose levels, culture, and gram stain [16]. Elevated CSF white blood cell count and protein levels are common findings in meningitis, while glucose levels are often decreased. CSF culture and gram stain are essential to identify the causative organism, guide antimicrobial therapy, and can be used to monitor response to treatment.

In addition to CSF analysis, imaging studies such as computed tomography (CT) or magnetic resonance imaging (MRI) may also be obtained to evaluate for complications of meningitis, such as hydrocephalus, cerebral edema, or abscess formation. However, these imaging studies are typically not used for the initial diagnosis of meningitis. CT is a strong consideration to be performed before lumbar puncture (LP) to exclude increased intracranial pressure (ICP) or mass lesion when CT is available and a patient has any of these criteria: immunocompromised state, history of CNS disease, new-onset seizure, papilledema, severe decreased consciousness (GCS<12) or focal neurologic deficit [6].

Blood cultures may also be obtained to help identify the causative organism and determine appropriate antimicrobial therapy. In particular, meningococcemia can rapidly lead to shock and multiorgan failure. Other laboratory tests, such as complete blood count (CBC), chemistry panel, and coagulation studies, are also routinely obtained to evaluate potential complications or comorbidities.

Rapid diagnostic tests, such as polymerase chain reaction (PCR) or antigen tests, may also be available in some settings. These tests can help quickly identify some causes of meningitis, such as bacterial or viral meningitis. They can provide near real-time speciation of the causative organism and help tailor appropriate treatment.

Table 3: CSF Testing Characteristics [9-11, 17-19]

Test	Normal Results	Bacterial Meningitis Results	Viral Meningitis Results	Fungal Meningitis Results
Appearance	Clear, colorless	Cloudy or turbid	Clear to slightly cloudy	Cloudy or turbid
WBC count	<5 cells/microliter	Elevated	Elevated, often lymphocytic	Elevated, often lymphocytic
Glucose	40-70 mg/dL	Decreased	Normal or slightly decreased	Decreased
Protein	15-45 mg/dL	Elevated	Normal to slightly elevated	Elevated
Gram stain	No organisms	Gram-positive or gram-negative organisms	Negative for bacteria, positive for virus	Negative for bacteria and virus
Culture	Negative	Positive for bacterial growth	Negative for bacteria, positive for virus	Positive for fungal growth

Risk Stratification

Several features in the history, physical examination, and testing can indicate a worse outcome in a patient with meningitis. Some of these include advanced age, altered mental status, presence of seizures, hypotension, tachycardia, high cerebrospinal fluid (CSF) protein and low glucose levels, high white blood cell count in CSF, and delayed initiation of appropriate antimicrobial therapy.
Various risk stratification tools have been developed for meningitis, such as the Glasgow Meningococcal Septicemia Prognostic Score (GMSPS), which is used to predict mortality in meningococcal disease. This tool includes variables such as age, Glasgow Coma Scale score, presence of meningismus, and presence of shock. This tool is most helpful in identifying the most sick cases, which are likely to be evident based on the clinical history and exam. Although this score exists, it is not routinely used in clinical practice. Another tool is the Bacterial Meningitis Score (BMS), which helps clinicians differentiate bacterial from aseptic meningitis based on the presence of certain clinical and laboratory features. The BMS includes age, cerebrospinal fluid protein level, cerebrospinal fluid neutrophil count, and peripheral blood absolute neutrophil count.

Management

In patients with whom you have concerns about meningitis, stabilization of an unstable patient is the priority. Assess the airway and breathing, including monitoring the respiratory rate and saturation levels. Administer supplemental oxygen if necessary. Evaluate circulation by checking the pulse, capillary refill time, and blood pressure. Provide fluids or administer medications as required. Next, the neurological function can be evaluated using tools like the Glasgow Coma Scale or AVPU (Alert, Verbal, Painful, Unresponsive) scale. Additionally, glucose levels and the presence of focal neurological signs, seizures, and papilledema should be assessed.

Empiric antibiotics should be started as soon as possible, even before the results of CSF culture and sensitivity are available, in order to reduce the risk of mortality and morbidity. In addition, supportive measures such as fluid and electrolyte management, seizure prophylaxis, and management of increased intracranial pressure are essential in managing meningitis. Patients with severe disease or complications may require ICU admission. Close follow-up with repeat CSF analysis and neuroimaging may be necessary to monitor response to treatment and identify potential complications.

Empiric treatment for bacterial meningitis typically involves using third-generation cephalosporins, such as ceftriaxone or cefotaxime, with or without vancomycin to cover for potential penicillin-resistant strains of Streptococcus pneumoniae. In infants under 1 month of age and patients over 50 years, ampicillin is often added to cover for Listeria monocytogenes [2]. Dexamethasone, a corticosteroid, is also given prior to or at the time of antibiotic initiation in adults and children with suspected or confirmed bacterial meningitis to reduce the risk of neurologic sequelae. The administration of corticosteroids has been shown to significantly reduce hearing loss and neurological complications in patients with meningitis.

However, using corticosteroids has not significantly impacted overall mortality rates [20]. The management of viral meningitis is mainly supportive. Antiviral treatment may be considered for specific viral pathogens, such as acyclovir for herpes simplex virus (HSV) or ganciclovir for cytomegalovirus (CMV). However, empiric antiviral treatment is not recommended in most cases of viral meningitis. The use of corticosteroids, such as dexamethasone, is controversial in viral meningitis and is not generally recommended [20].
Pre-exposure prophylaxis, though intrapartum prophylaxis of group B streptococcus in pregnant women, has significantly reduced the risk of early-onset group B strep meningitis [21]. Post-exposure prophylaxis is also an important consideration in contacts of patients diagnosed with meningitis; close contacts are defined as individuals who have had prolonged close contact with the index case, such as household contacts, healthcare workers, or individuals who shared a room or had direct contact with respiratory or oral secretions. Antibiotic prophylaxis is typically recommended within 24-48 hours of identification of the index case and may include rifampin, ciprofloxacin, or ceftriaxone, depending on the age and health status of the contact. In addition to antibiotics, vaccination with the meningococcal conjugate vaccine may be recommended for close contacts, particularly those at increased risk.

The recommended antibiotic prophylaxis is usually a single dose of intramuscular ceftriaxone (250 mg for adults and children weighing > 45 kg and 125 mg for children weighing < 45 kg). Alternatively, oral antibiotics such as rifampin, ciprofloxacin, or azithromycin can be used as alternatives. For exposure to Streptococcus pneumoniae, oral amoxicillin is recommended for prophylaxis, and for exposure to Haemophilus influenzae type b (Hib), rifampin or ceftriaxone is recommended.

Special Patient Groups

Elderly individuals, particularly those over 65, may present with atypical meningitis characterized by lethargy, minimal signs of meningismus, and the absence of fever. Conversely, younger individuals such as neonates, infants, and children often present with symptoms such as poor feeding, irritability, fever, and in babies, a shrill cry, decreased appetite, rash, and vomiting. In young children, the presentation of meningitis can mimic flu-like symptoms, including cough or respiratory distress, and it is not uncommon for them to have a history of respiratory tract infection. Seizures are also more frequently observed in this age group with meningitis. When evaluating a febrile child who appears unwell, it is crucial to consider bacterial meningitis as a potential diagnosis until ruled out. It is worth noting that blood and cerebrospinal fluid results may appear normal, especially in extremely young or old age groups.

When To Admit This Patient

Patients with suspected meningitis should be admitted to the hospital from the emergency department, as this is a potentially life-threatening condition that requires urgent evaluation and treatment. Admission should be considered for patients with a high likelihood of meningitis based on clinical presentation and laboratory findings. Patients with severe symptoms such as altered mental status, seizures, or signs of sepsis are particularly high-risk and should be admitted promptly. Patients with risk factors such as immunocompromised status, recent head trauma, or history of neurosurgical procedures should also be admitted.

Patients with meningitis who present with severe symptoms or complications such as altered mental status, seizures, respiratory distress, or signs of sepsis should be considered for admission to the intensive care unit (ICU). In addition, patients with bacterial meningitis or other severe forms of meningitis, such as fungal or tuberculous meningitis, and those immunocompromised should also be admitted to the ICU for close monitoring and aggressive treatment. Patients with a high risk of developing cerebral edema or increased intracranial pressure, such as those with hydrocephalus or brain abscess, may also require ICU admission. Close monitoring of vital signs, neurologic status, and laboratory parameters, such as blood glucose and electrolytes, is likely best done in an ICU.

Revisiting Your Patient

Let’s go back to the clinical presentation of your 21-year-old male refugee. He has fever, tachycardia, vomiting and confusion, and meningitis was suspected. You performed a lumbar puncture, and the cerebrospinal fluid analysis showed a white cell count of 1500 cells/µL with predominant neutrophils, protein level of 150 mg/dL, and glucose level of 30 mg/dL. The patient was started on treatment with intravenous ceftriaxone and vancomycin and admitted to the hospital. The patient was diagnosed with bacterial meningitis and was continued on intravenous antibiotics for a total of 14 days.

The patient responded well to the treatment and was discharged after completing the course of antibiotics. Appropriate public health notification was made, and the patient was scheduled for post-discharge follow-up care and vaccination.

Author

J. Austin Lee, MD MPH DTMH

Austin Lee, MD MPH DTMH, is a practicing emergency medicine doctor in the United States. He currently works with Indiana University Health, across several hospital sites. Dr. Lee obtained an MPH at the George Washington University before going to medical school at Indiana University. He completed his emergency medicine residency at the University of Virginia, and then worked at Brown University where he was a part of the Global Emergency Medicine fellowship. Austin has worked on a number of international emergency medicine projects, and is actively engaged in supporting the development of emergency medicine in Kenya.

Listen to the chapter

References

Tunkel AR, Scheld WM. Acute meningitis. In: Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 20th ed. Vol 1. New York, NY: McGraw-Hill Education; 2019:894-900.
Mandell GL, Bennett JE, Dolin R. Principles and Practice of Infectious Diseases. 8th ed. Vol 2. Philadelphia, PA: Elsevier; 2015:1116-1132.
Longo DL, Kasper DL. Bacterial meningitis. In: Longo DL, ed. Harrison’s Infectious Diseases. 3rd ed. New York, NY: McGraw-Hill Education; 2018:360-373.
World Health Organization. Defeating meningitis by 2030. Accessed May 25, 2023. https://www.who.int/initiatives/defeating-meningitis-by-2030.
GBD 2016 Meningitis Collaborators. Global, regional, and national burden of meningitis, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2018 Dec;17(12):1061-1082.
Parežnik A. Meningitis. October 12, 2018. Accessed May 25, 2023. https://iem-student.org/meningitis/.
McGill F, Heyderman RS, Panagiotou S, Tunkel AR, Solomon T, Connor MD. Acute bacterial meningitis in adults. The Lancet. 2016;388(10063):3036-3047.
Lu CH, Chang WN, Chang HW, et al. Adult bacterial meningitis in southern Taiwan: epidemiological trend and prognostic factors. J Neurol Sci. 2005;22(2):133-139.
van de Beek D, de Gans J, Spanjaard L, et al. Clinical features and prognostic factors in adults with bacterial meningitis. N Engl J Med. 2004;351(18):1849-1859.
Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis. 2004;39(9):1267-1284.
van de Beek D, de Gans J, Tunkel AR, et al. Community-acquired bacterial meningitis in adults. N Engl J Med. 2006;354(1):44-53.
McGill F, Griffiths MJ, Solomon T. Viral meningitis: current issues in diagnosis and treatment. Curr Opin Infect Dis. 2017 Apr;30(2):248-256.
Góralska K, Blaszkowska J, Dzikowiec M. Neuroinfections caused by fungi. Infection. 2018 Aug;46(4):443-459.
Pana A, Vijayan V, Anilkumar AC. Amebic Meningoencephalitis. 2023 Jan 21. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan
Iguchi M, Noguchi Y, Yamamoto S, Tanaka Y, Tsujimoto H. Diagnostic test accuracy of jolt accentuation for headache in acute meningitis in the emergency setting. Cochrane Database Syst Rev. 2020 Jun 11;6(6):CD012824.
Roberts JR, Custalow CB, Thomsen TW. Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Care. Elsevier; 2018.
Kumar R, Bose M, Singh SN, et al. Clinicoradiological and neurophysiological correlation in Japanese encephalitis. Ann Trop Paediatr. 1994;14(4):311-318.
González-Duarte A, Cárdenas G, Torres-Narbona M, et al. Cerebrospinal fluid lactic acidosis in aspergillosis meningitis. Arch Neurol. 2007;64(9):1362-1364.
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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Delirium and Dementia (2024)

November 12, 2024November 13, 2024 ~ iEM Education Project Team ~ Leave a comment

by Lo Lucian Simeon, Ngai Oona Wing Yan, & Lo Yat Hei

You have a new patient!

Adam is a 76-year-old man who is brought to the emergency room by his family members, complaining of a lack of responsiveness and general lethargy. According to his family, Adam has been having increasing memory problems in the past year and has gotten lost while walking around his neighborhood multiple times. His personality has changed and becomes agitated easily. He is also becoming less attentive to personal hygiene, wearing dirty clothes for several days, and having several episodes of urinary incontinence. Today, his family members noted that he had fallen asleep multiple times and showed no interest in his food. He did not respond when addressed by name. At the time of presentation, he is conscious, but appears lethargic and uncooperative. He cannot tell where he is and does not seem to recognize his family members. His past medical history includes hypertension and hypercholesterolemia. He is taking amlodipine and simvastatin.

Vitals show a heart rate of 108 beats per minute, blood pressure 154/84 mmHg, temperature 36.7℃, respiratory rate 20 breaths per minute, and an oxygen saturation of 98% on room air. His Glasgow coma score is E4V4M6.

What do you need to know?

Importance

Dementia and delirium are two medical conditions that significantly impact the health and well-being of older adults and their families. In this case, Adam’s symptoms suggest that he may be experiencing one or both of these conditions, and it is important to understand their relevance in clinical practice.

Dementia is defined as an acquired global decline in cognitive function, affecting one’s memory, language, learning, and behavior without impairment of consciousness. Dementia is associated with a gradual, progressive decline. It is a leading cause of disability and dependence among older adults, with advancing age being one of the most significant risk factors [1]. With the global population aging, the number of individuals living with dementia is expected to rise significantly. The World Health Organisation estimates that 47 million people worldwide live with dementia, and this number is expected to triple by 2025 [2].

Delirium, conversely, is a clinical syndrome characterized by an acute state of confusion, inattention, and cognitive impairment. It can occur in people of any age, but is particularly common among the older population and hospitalized patients [1]. Delirium can wax and wane over time, unlike dementia, which is more progressive and persistent.

Dementia and delirium pose a tremendous burden not only on patients and caregivers, but also on our healthcare system and society. Therefore, understanding the significance of dementia and delirium is crucial in clinical practice. Identifying and managing these conditions early improves clinical outcomes and optimizes quality of life.

Epidemiology & Pathophysiology

Dementia is a condition that is more commonly seen in older individuals, with the incidence increasing from the age of 65. An exception is frontotemporal dementia, a rare type of dementia that is usually diagnosed from the age of 40 to 60. The most prevalent type of dementia is Alzheimer’s disease, which accounts for 60-80% of all cases. Other neurodegenerative dementias, such as vascular dementia, dementia due to Lewy bodies, Parkinson’s disease, and frontotemporal dementia, account for the remaining cases [3].

The underlying pathophysiology of dementia varies depending on the type and subtype, with most types involving damage to neurons and their connections in the brain. Abnormal protein accumulation is a common feature for many types of dementia, including amyloid and tau in Alzheimer’s disease, Lewy bodies with alpha-synuclein protein in Lewy body disease, and mutations causing the deposition of TDP-43 and tau proteins in frontotemporal dementia. Other factors, such as ischemic injury, HIV infection, and alcohol consumption, can also lead to cytotoxic processes in the brain and contribute to the development of dementia [4].

On the other hand, the epidemiology of delirium is more complex as it varies depending on age and underlying medical conditions. Although delirium is more prevalent in older individuals, with rates increasing after the age of 70, it is also common in younger patients suffering from chronic illnesses such as cardiovascular and renal comorbidities, dementia, or psychiatric illnesses [5].

The pathophysiology of delirium can result from various physiological and structural lesions in the brain. While its mechanisms are not fully understood, delirium can be caused by neurotransmitter imbalances, brain lesions involving the ascending reticular activating system, as well as disrupted blood-brain barrier function that causes the leakage of neurotoxic agents into the brain. Patients with impaired cholinergic transmission, such as those with Alzheimer’s disease, are particularly susceptible to delirium caused by medication use. Additionally, delirium can result from alcohol abuse, drug withdrawal, mental illnesses, psychosocial stress, and sleep deprivation [6].

Epidemiological and pathophysiological data on dementia and delirium allow physicians to identify individuals at risk and intervene appropriately. Since the development of dementia and delirium are multifactorial and the pathophysiology is variable among patients, evaluating and treating delirium and dementia is based on clinical gestalt and the presumed underlying cause.

Medical History

Dementia and delirium are two diagnoses that must be considered in elderly patients presenting with cognitive change to the emergency department. Differentiation between the two conditions is based on features noted in the history and physical examination. Table 1 lists symptoms that can help differentiate between the two conditions.

Delirium typically presents with sudden onset of impaired awareness, confusion, clouding of consciousness, and disturbances of perception (e.g., illusions or hallucinations). Delirium should be suspected when there is an acute deterioration in behavior, cognition, and daily functioning [7]. Delirious patients usually have short-term memory issues and may be disoriented by time and place. Abnormalities of cognition and behavior can fluctuate over brief periods. The level of awareness may range from hypervigilant and agitated to blunt and unreactive. The patient’s speech may be incoherent, nonsensical, or tense. The patient usually has no discernible focal neurological defect [8].

Dementia has various presentations according to the specific types, but symptoms often overlap. Alzheimer’s dementia, the most common type, presents with a history of a chronic, steady decline in cognitive ability, especially memory. It is often associated with difficulties in social relationships, activities of daily living, and work. During the early stages of dementia, clinical presentations can be quite subtle, and patients may try to hide their cognitive impairments [9].

Patients who present to the emergency department with symptoms of dementia are most likely in the later stages of disease progression. Acute presentation of dementia is possible in vascular dementia, and this subtype may present with symptoms of focal neurological deficit. Patients who are demented typically do not present with any impairment of consciousness. However, acute episodes of delirium can be superimposed on patients who have dementia. For example, Lewy body dementia can present with fluctuating levels of consciousness. Diagnosing uncommon variants poses a challenge to emergency physicians and is often done only after referral to a neurologist [10].

Obtaining a thorough history is essential in diagnosing delirium and dementia. Unfortunately, delirious or demented patients are often disoriented and cognitively impaired, resulting in the inability to provide accurate information about their condition. A detailed history should be obtained from family, caregivers, and healthcare staff (nurses, healthcare assistants, and other allied health professionals).

Important features to note during history are the onset of symptoms, factors that worsen or improve symptoms, drug or alcohol use, pre-existing endocrine or psychiatric disorders, exposure to toxins or traumatic injury, social history, and previous similar episodes of confusion or altered mental status. Drug history is particularly important as the use of drugs that impair cognition (e.g., analgesics, anticholinergics, psychotropic medications, and sedatives) may explain the presenting symptoms.

Determining the onset of symptoms, in particular, for patients with dementia, can be difficult due to the gradual nature of the disease. Questions like, “When did you first notice the memory loss?” and “How has the memory loss progressed since then?” can give a general idea on the patient’s current condition. The patient’s social history, especially work, educational history, and ability to conduct activities of daily living, can help establish a baseline for the patient.

Table 1: Key symptoms to look for to differentiate between delirium and dementia during history taking [11]

	Delirium	Dementia
Onset	Acute	Insidious/chronic
Course	Fluctuating	Progressive
Duration	Days to weeks	Months to years
Consciousness	Altered	Clear
Alertness	Impaired	Normal, except for in severe cases of dementia
Behaviour & Speech	Agitated/withdrawn/ depressed/combination of symptoms	Intact early on

Typical presentations of dementia of various type

Dementia manifests in various forms, each with distinct characteristic presentations. Alzheimer’s dementia typically involves memory loss, mood instability, apathy, and may include depressive or paranoid features. Additionally, patients may experience apraxia, anosognosia, sensory inattention, and progressive personality and intellectual deterioration. Vascular dementia, on the other hand, often has an abrupt onset with a stepwise deterioration and a fluctuating course. It is marked by slowed thinking, difficulties in organization, preserved personality and insight, and may include focal neurological deficits. Dementia with Lewy bodies is characterized by Parkinsonism, cognitive and alertness fluctuations, as well as visual hallucinations, delusions, and autonomic dysregulation. Frontotemporal dementia commonly occurs at a younger age, typically between 40 and 60 years, and is associated with early personality changes, disinhibition, and overactivity.

Physical Examination

The physical exam of the dementia and delirium patient starts with taking vital signs, assessing the airway, breathing, circulation, and performing a focused neurological exam. Calculating the Glasgow Coma Score (GCS) and checking blood glucose should be checked on all patients with behavioral or cognitive changes.

Table 2 lists the key signs of differentiating delirium and dementia. Key features such as acute onset, fluctuations in awareness, orientation, and consciousness, cognitive decline, and potential sensory disruptions can help distinguish delirium from dementia. This includes declining memory function, language ability, and judgment. When in doubt, the general rule of thumb is to assume the patient is having an episode of delirium and try to rule out the common causes. This rule can be applied even for patients with known psychiatric illnesses like depression and dementia, as they are also susceptible to delirium superimposed on their existing condition.

Table 2: Key signs to look for to differentiate between delirium and dementia during physical exam [11]

	Delirium	Dementia
Conscious level	Abnormal	Normal
Psychomotor changes	Increased/decreased	Often normal
Reversibility of symptoms	Reversible usually	Irreversible

On neurological examination, look for signs of stroke, parkinsonism, gait abnormalities, and abnormal eye movements. Dementia caused by Alzheimer’s disease generally has no sensory or motor deficits. Whereas for delirium, it is essential to identify any co-existing neurological disorders that may cause a presentation of delirium. Special tests for gait, daily living, and cognitive function assessment should be done to assess the severity of the patient’s condition. A thorough physical examination of other systems should also be conducted to look for signs of encephalopathy and drug and alcohol abuse.

Use the physical exam to help identify any exacerbations of an underlying medical illness (e.g., signs of diabetic ketoacidosis in a diabetic patient) and to evaluate for signs that may reveal an underlying cause. For example, a high fever, low blood pressure, rapid or slow heart rate, difficulty breathing, severe pain, or malaise may indicate delirium caused by an infection, sepsis, or shock that requires immediate medical attention. Severe thirst, nausea, and vomiting may indicate dehydration or electrolyte disturbances that should be promptly treated. Signs of unresponsiveness, difficulty breathing, or seizures may indicate intracranial bleeding or alcohol or drug intoxication. Since these conditions can cause delirium and have symptoms that overlap with dementia, it is important to prioritize and appropriately manage these urgent and life-threatening cases [12].

Alternative Diagnoses

Table 3 shows alternative diagnoses to consider when evaluating for dementia and delirium. In patients presenting with altered cognitive levels, life-threatening causes that need to be ruled out include hypoglycemia, electrolyte abnormalities such as hyponatremia and hyperkalemia, dehydration, stroke, intoxication/overdose, encephalopathy, cerebral infection, sepsis, and shock.

Psychiatric disorders such as psychosis, schizophrenia, and depression are among the list of differential diagnoses that could present with similar symptoms. Frequently, in patients with delirium, they do not have any previous history of psychiatric illness. In delirium, hallucinations and illusions are acute or subacute and fluctuate over time. In addition, the patient has impaired memory, orientation, and judgment, as well as clouding of consciousness. Elderly patients with a depressed mood, hopelessness, and suicidal ideation may be suffering from “pseudodementia” (false dementia). When the symptoms of depression are treated, the dementia-like condition usually resolves itself [13].

Investigations, such as bloodwork, toxicology screening, biochemical tests, and imaging can help determine a delirium patient’s underlying cause and identify an alternative diagnosis. Investigations to consider are listed below under “Acing diagnostic testing.”

Table 3: Alternative diagnoses of altered cognitive level [14]

Central nervous system: brain abscess, cerebral neoplasm, encephalitis, intracranial haemorrhage, meningitis, normal pressure hydrocephalus, variant Creutzfeldt-Jakob Disease and bovine spongiform encephalopathy

Electrolyte: hyper/hypocalcemia, hyperkalemia, hyper/hyponatremia

Dehydration

Environmental: heat stroke, snake bite

Infective: sepsis, rabies, malaria

Metabolic: diabetic ketoacidosis, hyperosmolar hyperglycemic nonketotic coma, hypoglycemia, hypothyroidism, uremia, hepatic encephalopathy

Nutrition deficiency: folate, thiamine (Wernicke encephalopathy), vitamin B12,

Poisoning: amphetamine, anticholinergic, antidepressant, cocaine, hallucinogen, lithium, tricyclic antidepressant, valproate, withdrawal

Psychiatric: depression, psychosis

Transient global amnesia

Acing Diagnostic Testing

Initial Investigations

Complete Blood Count with Differential: This test is critical for assessing overall health and detecting a variety of conditions, such as infections, anemia, and blood disorders. The differential component provides a breakdown of different types of white blood cells, which can help to identify specific types of infections (e.g., bacterial or viral) and help diagnose other hematological disorders like leukemias or other abnormalities in blood cell production.
Electrolyte Panel: The electrolyte panel is essential for assessing the balance of minerals in the body, such as sodium, potassium, calcium, and chloride. Disturbances in these levels can indicate a variety of issues. For instance, hyponatremia (low sodium) can be a sign of dehydration or kidney dysfunction, while hyperkalemia (high potassium) could indicate kidney failure or metabolic acidosis. These imbalances can have significant effects on muscle function, nerve transmission, and overall cellular processes.
Liver Function Test: Liver function tests are crucial in diagnosing liver diseases such as hepatitis, cirrhosis, and alcoholic liver disease, as well as conditions like hepatic encephalopathy. These tests measure the levels of enzymes, proteins, and substances like bilirubin, which indicate how well the liver is working. Abnormal results may suggest liver damage, bile duct obstruction, or liver dysfunction that can lead to brain symptoms, especially in severe cases of hepatic encephalopathy.
Renal Function Test: This test evaluates how well the kidneys are filtering waste from the blood. It includes measurements like serum creatinine and blood urea nitrogen (BUN), which are key indicators of kidney function. Elevated levels may suggest renal failure, and abnormalities in these values can also help diagnose uremia, a condition where kidney dysfunction leads to the accumulation of waste products in the blood, potentially affecting multiple organ systems.
Blood Sugar: Blood sugar levels are measured to rule out conditions like hypoglycemia (low blood sugar) and hyperglycemia (high blood sugar). In patients with diabetes, particularly in cases of diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic nonketotic syndrome (HHNS), these levels can be critically elevated and require immediate treatment. Monitoring blood sugar is essential for managing and preventing complications related to these conditions.
Urine Dipstick: The urine dipstick test is a quick and convenient method for identifying potential urinary tract infections (UTIs), which are a common cause of sepsis in elderly patients. It can detect substances like white blood cells, nitrites, and protein in the urine, all of which suggest infection or inflammation. Early detection of UTIs is crucial, as they can quickly progress to sepsis if untreated.
Chest X-ray: A chest X-ray is an important imaging tool for identifying lung consolidation, a hallmark of chest infections such as pneumonia. Pneumonia is another common cause of sepsis, particularly in elderly patients with weakened immune systems. The X-ray can also help detect other lung-related issues like fluid accumulation, pulmonary edema, or lung tumors that could complicate the clinical picture.
CT Scan of the Brain: A CT scan of the brain is used to identify structural abnormalities, including the presence of tumors, stroke, or brain hemorrhages. It is also used to detect cerebral atrophy (shrinkage of brain tissue) and ventricular enlargement, which can be indicative of conditions like dementia. This imaging modality is important in diagnosing neurological disorders and guiding further management for patients with cognitive or neurological impairments.

Further Investigations If A Differential Is Suspected

Urine and Blood Toxicology: This test is performed to detect the presence of drugs, alcohol, or other toxic substances in the body. Toxicology screens can identify intentional or unintentional overdoses, exposure to toxic substances, and drug or alcohol misuse. In cases of altered mental status or cognitive impairment, toxicology testing helps to rule out substance-induced confusion or delirium, which can mimic other medical or psychiatric conditions.
Thyroid Function Test: Thyroid hormones play a significant role in regulating metabolism and overall brain function. Abnormal thyroid function, whether hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid), can lead to symptoms of cognitive impairment, mood changes, and lethargy. A thyroid function test measures levels of thyroid hormones (such as TSH, T3, and T4) to determine if an imbalance is contributing to the patient’s cognitive or neurological symptoms, which can be reversible with appropriate treatment.
Vitamin B12 and Folate Levels: Both Vitamin B12 and folate are essential for nerve function and the production of red blood cells. A deficiency in either of these vitamins can lead to cognitive impairment, memory loss, and other neurological symptoms. Vitamin B12 deficiency, in particular, is known to cause a condition called subacute combined degeneration of the spinal cord and brain, which can lead to irreversible damage if left untreated. Checking these levels helps to rule out nutritional deficiencies as a potentially treatable cause of cognitive decline.
Bacteriology and Viral Detection: Infection-related causes of cognitive impairment or altered mental status may be identified through bacteriology and virology testing. This typically involves blood and urine microscopy, as well as culture tests to detect bacterial, viral, or other pathogenic organisms. Infections, especially in elderly or immunocompromised patients, can lead to sepsis or encephalitis, which can significantly impact cognitive function. Identifying and treating an underlying infection can prevent further deterioration and improve cognitive outcomes.

Risk Stratification

Cognitive assessment tools help identify and grade abnormal cognitive performances. They can also be integrated into the emergency medicine physical exam to screen patients for mild cognitive impairment or dementia.

Instead of an extended mental status examination or formal neuropsychological testing, more focused screening tools are more relevant and feasible for use in the emergency department [15]. Examples of screening tools validated for use in the emergency department include the abbreviated mental test score (AMTS) and its abbreviated four-item version (AMT4), the mini-mental state examination (MMSE), and the Montreal Cognitive Assessment (MoCA). They assess a broad range of cognitive domains, including memory, language, and orientation. These tests are designed to be administered in 15 minutes or less and have pre-determined cut-off scores to help distinguish patients with normal cognitive function and those with impaired cognitive function [16].

These screening tools are intended to help screen individuals who may require more extensive neurological assessments. They should only be used as a reference and must be integrated with history and physical examination findings for a holistic approach. Multiple factors, such as altered mood, disorientation, and education level, can affect the accuracy of these screening tools.

Table 4: Abbreviated mental test score four-item version (AMT4)

Ask the patient to state each of the following. A score less than 4 should prompt further cognitive screening.
Age	Correct (+1) / Incorrect (0)
Date of birth	Correct (+1) / Incorrect (0)
Place	Correct (+1) / Incorrect (0)
Year	Correct (+1) / Incorrect (0)

Management

The ABCDE approach is used for the initial management of patients with cognitive changes, behavioral changes, and alterations in consciousness, which may be present in delirium or dementia.

The acute management of dementia and delirium is variable and depends on the patient’s underlying medical conditions and presenting symptoms. The main goal of managing dementia and delirium in the emergency department is to identify and treat any life-threatening underlying causes. Based on the patient’s signs and symptoms, a thorough history, physical exam, and pertinent investigations should be ordered. Patient and staff safety should also be prioritized, as these patients may be aggressive and combative.

Obtaining investigations to evaluate for the underlying cause may be hindered by the patient’s aggressive and combative state. If this is the case, the first attempt is to calm the patient and de-escalate the situation verbally. If unsuccessful, chemical sedation should be considered for the safety of the patient and the healthcare staff. Examples of chemical sedation used in an emergency department setting include benzodiazepines, antipsychotics, and dexmedetomidine [17,18]. Close monitoring is necessary after the patient is sedated. Sedatives should be used only when necessary, as they have the potential to worsen delirium and disorientation.

Physical restraints and environmental seclusion are other adjunctive treatments for agitated delirium or dementia patients. However, their use should be weighed with the psychological and physical risks they may cause (e.g., emotional distress, skin and soft tissue injuries, orthopedic injuries, rhabdomyolysis, etc.). Alternative methods of managing agitation should always be attempted prior to physical restraint, such as explaining your desire to care for the patient, orienting the confused patient to his or her surroundings, using verbal de-escalation techniques, providing psychosocial support, and relocating to a calm and quiet environment, if possible [19].

Special Patient Groups

Most patients presenting with delirium and/or dementia are elderly patients. Younger patients (<60 years) presenting with delirium or patients who have rapidly progressing dementia may require extensive evaluation to discover the underlying cause. Further investigations could include lumbar puncture, electroencephalography, advanced neuroimaging, neuropsychological, and genetic testing [20]. Regardless of age, the most common causes of early-onset dementia are still Alzheimer’s disease, vascular dementia, and frontotemporal dementia [21].

When To Admit This Patient

Admission of dementia and delirious patients depends on various factors, including the severity of symptoms, comorbidities, and safety concerns. Patients who present with acute changes in their mental status, such as sudden confusion or agitation, should be further assessed for any underlying medical conditions and often require hospitalization. Delirious patients, particularly those with severe symptoms or who are at risk of harming themselves and others, should also be admitted until stabilized. Ultimately, the decision to admit dementia and delirious patients in an emergency department setting should be based on a comprehensive evaluation of the patient’s medical history, current symptoms, and risk factors.

The patient who is coming to the emergency department for a chronic presentation of Alzheimer’s dementia could be discharged if life-threatening conditions have been ruled out and home safety is not a concern. They should be referred to an outpatient primary care doctor or a geriatrician for follow-up and prescription medications to manage behavioral symptoms. Be sure to educate the patient’s family members on the diagnosis and to monitor for any new or worsening symptoms that may require urgent medical attention. Advise the family on managing certain scenarios, prioritizing the patient’s basic daily needs, addressing any medical concerns, and maintaining patient and family safety. Refer the patient to a geriatric community support program, if available.

Revisiting Your Patient

Adam’s initial vital signs are stable, and you have decided to continue his management in the consultation room. His history of cognitive and behavioral change over the past year is consistent with dementia. However, his acute presentation of impaired consciousness level and disorientation raises your suspicion of concurrent delirium from an underlying medical condition. Collateral history from the family indicates that Adam lives with his wife, who is 85 years old and limited in her ability to assist Adam with his daily needs. Focused drug and alcohol history is unrevealing.

Further neurological exams do not identify any focal neurological signs or gait disturbance. Physical examinations of the cardiovascular, respiratory, and abdomen are unremarkable. Blood glucose is within the normal range. Due to his disorientation, his Glasgow coma score is 14 (E4/V4/M6).

You consider using AMT4 to screen for cognitive impairment. He can recall his age and date of birth and tell where he is, but he fails to tell us the current year. You establish that he has delirium with impaired alertness and likely an underlying cognitive impairment.

You decide to conduct further investigation to look for potential underlying causes, especially those which may prompt immediate treatment. You arrange blood tests, including complete blood count, electrolytes, liver, and renal function tests, in consideration of potential sepsis, electrolyte disturbance, and acute organ failure. You arrange a CT brain to rule out any acute cerebral hemorrhage and space-occupying lesion. Chest X-ray and ECG are performed, as well. As you order these investigations, you consider that the patient may become agitated and uncooperative during these tests, so you review options for chemical sedation should they be needed.

You discuss openly with Adam and his family on his diagnosis of delirium and likely dementia. Your preliminary investigations show a urinary tract infection; one dose of intravenous antibiotics has been ordered. You suggest admitting Adam for monitoring and investigations due to safety concerns and his inability to care for himself due to his recent rapid decline. You discuss the importance of appropriate follow-up care and geriatric resources specializing in dementia. The patient is admitted to the general medical floor for further testing and monitoring.

Authors

Lo Lucian Simeon

Lucian Lo is a medical student at The Chinese University of Hong Kong. An avid enthusiast of emergency medicine and humanitarian work, he hopes to one day combine his two great passions as a front-line healthcare professional in conflict and disaster zones. He is a certified Advanced Medical Life Support Provider and Youth Mental Health First Aid Provider. In addition, he has led and organized multiple medical service projects in Hong Kong, Nepal, and Thailand. In regard to emergency medicine, his interests include trauma care, intensive care medicine, and pre-hospital emergency medicine.

Ngai Oona Wing Yan

Oona Ngai is a medical student at The Chinese University of Hong Kong with a passion for emergency medicine and humanitarian work. She has organized and participated in various volunteer services for vulnerable communities in Hong Kong, including the homeless, refugees, and domestic helpers. Oona is also a St. John’s certified Advanced Medical Life Support Provider and aspires to better equip herself with the necessary skills and knowledge to provide effective medical care in emergency situations. In addition, she has published a life story book on rare diseases to raise awareness and advocate for those in need.

Lo Yat Hei

Dr. Lo Yat Hei is an emergency physician who is trained and grew up in Hong Kong. He now serves at the Accident and Emergency Department of Prince of Wales Hospital and teaches at the Accident and Emergency Medicine Academic Unit of the Chinese University of Hong Kong. When not practicing medicine, he enjoys gardening, ceramics and playing mahjong.

Listen to the chapter

References

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). American Psychiatric Association; 2013.
World Health Organization. “Dementia.” Fact Sheet, https://www.who.int/news-room/fact-sheets/detail/dementia.
Ljubenkov PA, Geschwind MD. Dementia. Semin Neurol. 2016;36(4):397-404. doi:10.1055/s-0036-1585096
Plum F. The pathophysiology of dementia. Gerontology. 1986;32 Suppl 1:67-72. doi:10.1159/000212832
Wilson JE, Mart MF, Cunningham C, et al. Delirium [published correction appears in Nat Rev Dis Primers. 2020 Dec 1;6(1):94]. Nat Rev Dis Primers. 2020;6(1):90. Published 2020 Nov 12. doi:10.1038/s41572-020-00223-4
Maclullich AM, Ferguson KJ, Miller T, de Rooij SE, Cunningham C. Unravelling the pathophysiology of delirium: a focus on the role of aberrant stress responses. J Psychosom Res. 2008;65(3):229-238. doi:10.1016/j.jpsychores.2008.05.019
Fong TG, Tulebaev SR, Inouye SK. Delirium in elderly adults: diagnosis, prevention and treatment. Nat Rev Neurol. 2009;5(4):210-220. doi:10.1038/nrneurol.2009.24
Avelino-Silva TJ, Campora F, Curiati JAE, Jacob-Filho W. Prognostic effects of delirium motor subtypes in hospitalized older adults: A prospective cohort study. PloS one. 2018;13(1):e0191092. doi:10.1371/journal.pone.0191092
Emmady PD, Schoo C, Tadi P. “Major Neurocognitive Disorder (Dementia).” In: StatPearls. StatPearls Publishing; 2023. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557444/
Morandi A, Davis D, Bellelli G, et al. The Diagnosis of Delirium Superimposed on Dementia: An Emerging Challenge. J Am Med Dir Assoc. 2017;18(1):12–18. doi:10.1016/j.jamda.2016.07.014
Han JH, Suyama J. Delirium and Dementia. Clin Geriatr Med. 2018;34(3):327-354. doi:10.1016/j.cger.2018.05.001
Han JH, Wilson A, Ely EW. Delirium in the older emergency department patient: a quiet epidemic. Emerg Med Clin North Am. 2010;28(3):611-631. doi:10.1016/j.emc.2010.03.005
Brodaty H, Connors MH. Pseudodementia, pseudo-pseudodementia, and pseudodepression. Alzheimers Dement. 2020;12(1):e12027. doi:10.1002/dad2.12027
Ross GW, Bowen JD. The diagnosis and differential diagnosis of dementia. Med Clin North Am. 2002;86(3):455-476. doi:10.1016/s0025-7125(02)00009-3
Carpenter CR, Banerjee J, Keyes D, et al. Accuracy of Dementia Screening Instruments in Emergency Medicine: A Diagnostic Meta-analysis. Acad Emerg Med. 2019;26(2):226-245. doi:10.1111/acem.13573
Nasreddine ZS, Phillips NA, Bédirian V, et al. The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc. 2005;53(4):695–699. doi:10.1111/j.1532-5415.2005.53221.x
Barr J, Fraser GL, Puntillo K, et al. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Critical Care Medicine. 2013;41(1):263-306. doi: 10.1097/CCM.0b013e3182783b72
Hall JE, Uhrich TD, Barney JA, Arain SR, Ebert TJ. Sedative, amnestic, and analgesic properties of small-dose dexmedetomidine infusions. Anesth Analg. 2000;90(3):699-705. doi: 10.1097/00000539-200003000-00033
Lightfoot CB, Breden C, Moczygemba LR. Delirium: diagnosis, prevention and management. Am J Health Syst Pharm. 2017;74(18):1365-1375. doi: 10.2146/ajhp160950
Lempert T, Schmidt D, Rosemeyer J. Psychogenic nonepileptic seizures: a guide. J Neurol Neurosurg Psychiatry. 2006;77(2):297-303. doi:10.1136/jnnp.2005.082149.
Rossor MN, Fox NC, Mummery CJ, Schott JM, Warren JD. The diagnosis of young-onset dementia. Lancet Neurol. 2010;9(8):793–806. doi:10.1016/S1474-4422(10)70159-9

Reviewed and Edited By

Joseph Ciano, DO, MPH, MS

Arif Alper Cevik, MD, FEMAT, FIFEM

Seizure: Lethal Dissection

November 15, 2021October 30, 2021 ~ Naveen Paila, India ~ 1 Comment

Case Presentation

A 49-year old female without any co-morbidities presented to the emergency department (ED) with seizures. On arrival, she was in a postictal state.

She had recently visited a local hospital with complaints of severe dysmenorrhea and low back pain. The attenders informed us that she was very sleepy and weak at that time, was treated for pain and given tranexamic acid, and sent home. The next day, she had one episode of Generalized Tonic-Clonic Seizure, and she arrived in our ED in a postictal phase. She vomited twice in the ED.

Her vitals were as follows:

Blood pressure (BP): 160/100 mmHg.
Heart rate (HR): 22/min
Peripheral capillary oxygen saturation (SPO2): 98% on room air
General Random Blood Sugar (GRBS): 233 mg/dl
Glasgow Coma Scale (GCS): E2V5M6

Her examination was as follows:

The patient was drowsy but arousable.
Pupils bilateral reacting to light. No anisocoria.
CNS examination could not be completed as the patient was drowsy.
A normal pattern of breathing. The respiratory examination was normal.
The abdomen was soft, symmetric, and non-tender without distention.

Point-of-care ultrasound (POCUS) showed a flap in the abdominal aorta. (See Figure 1 and 2 for transverse and longitudinal views of the aorta, respectively) Upon this finding, cardiac surgery and neurology consultations were sought.

Image shows transverse section of the abdominal aorta showing a flap.

Image shows abdominal aorta showing a flap.

The laboratory results were as follows:

D-dimer: 1192 ng/ml
Haemoglobin (Hb): 10 g/dl
The international normalized ratio (INR): 1.25
Platelets: 260000 per mcL
Total leucocyte count (TLC): 22000 cells/mm3
Creatinine :1.6 mg/dl.

Meanwhile, the patient was suffering multiple seizure-like episodes, characterized by staring, deviation of the mouth, and irregular limb movements, but these episodes lasted for few minutes and ended without the postictal phase. The patient was drowsy but obeyed commands and did not have any recollection of those few minutes.

Head computed tomography (CT) showed no infarct or bleeding. It was normal.

CT angiogram and aortogram revealed that the patient had Stanford Type A aortic dissection with the flap extending to the entire left subclavian artery, with severely occluding filling defects and thrombosis of the false lumen into bilateral common carotid arteries (See Figure 3, 4 and 5). On the other end, the dissection extended to the common iliac arteries (See Figure 6).

Image shows CT Aortogram showing bilateral common carotid artery filling defects

And on the other loose of the string the dissection was extending till the common iliac arteries.

Image shows ascending and descending aortic dissection

Image shows dissection of the common iliac artery before bifurcation.

Management

Initially, the patient was treated symptomatically by anti-epileptics and analgesics. After the cardio-thoracic and vascular surgeon consultations, we decided to airlift the patient to a higher centre as our hospital was tertiary care and there were no grafts for the urgent repair of the extensive aortic dissection. We intubated the patient for secure transportation. However, we learned that the patient expired in the higher centre before reaching the operating room.

Discussion

Before I shed light on the important part of this discussion, I know that the outcome of this case was unfortunately grave. However, I chose this case because of it.

In this case, the patient had low back pain in her previous hospital visit. However, she was sent home with symptomatic management, implying that it could have been addressed more carefully. She visited our ED one day later, and POCUS let us diagnose the dissection in 15 minutes, which was confirmed by a CT aortogram within 40 minutes. After consultations and finding the available facility, we airlifted the patient to a higher centre for urgent repair, but the patient could not make it to the operating room.

We all know acute aortic dissection is the most common life-threatening disorder affecting the aorta. Over the first several hours, the mortality rate increase up to 1% per hour; therefore, early intervention is critical (1). In our case, the involvement of bilateral carotid arteries caused seizure-like episodes and altered mental status. Also, studies show that patients with similarly located dissections may experience neck pain, transient ischemic attacks (TIA), cerebral ischemia, transient monocular blindness and subarachnoid haemorrhage (SAH) but not seizure(2). In our case, the global hypo-perfusion caused recurrent TIAs, which resembled seizure-like clinical episodes. That’s why emergency physicians should be vigilant about the underlying causes of seizure-like activities, even if altered mental status similar to postictal state is present, especially if the patient does not have a history of seizures and the complaints are unclear. Keep the aortic dissection in mind as a differential. Also, I cannot stress the use of POCUS in the ED enough. It is a game-changer, and in our case, it detected a lethal disease successfully.

Learning Points

Never ignore back pain that does not subside after adequate pain management.
POCUS is always a game-changer. It saves a lot of time and lives, as in my case.
Seizures or not, you must keep a high suspicion for lethal vascular diseases. Remember the basics: If unclear, go back to history.
Once you confirm an aortic dissection, never delay treatment because time = life.
Never ever send a patient back home unless you are completely sure about the cause of the presenting symptom. Over investigating is ok when compared to under investigating, when it might cost a life.

References and Further Reading

Braverman AC. Acute aortic dissection: clinician update. Circulation. 2010;122(2):184-188. doi:10.1161/CIRCULATIONAHA.110.958975
Debette S, Grond-Ginsbach C, Bodenant M, et al. Differential features of carotid and vertebral artery dissections: the CADISP study. Neurology. 2011;77(12):1174-1181. doi:10.1212/WNL.0b013e31822f03fc

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Question Of The Day #53

September 3, 2021June 19, 2021 ~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most likely cause for this patient’s condition?

Explanation

This patient endured a high-speed motor vehicle accident, arrives with hypotension and bradycardia, and has a C6 vertebral body fracture on imaging. These details support a diagnosis of neurogenic shock, a type of distributive shock.

Shock is an emergency medical state characterized by cardiovascular or circulatory failure. Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure. Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic. The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap. The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam. Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management. The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.

Neurogenic shock is caused by spinal cord damage above the T6 level. Unlike other types of shock, neurogenic shock is characterized by hypotension and bradycardia (not tachycardia). These vital sign abnormalities are caused by damage to sympathetic nervous system (Choice C). Neurogenic shock has decreased systemic vascular resistance (warm extremities), not increased systemic vascular resistance (cool extremities) (Choice A). Occult hemorrhage (Choice B) is always a concern in a trauma patient. However, this would present with findings of hypovolemic/hemorrhagic shock (tachycardia, hypotension, cool extremities). Tension pneumothorax (Choice D) is also unlikely as the patient has clear bilateral lung sounds on exam. The best answer is Choice C.

References

Morgenstern J. (2015). An approach to undifferentiated hypotension. First10EM. Retrieved from https://first10em.com/undifferentiated-hypotension/
Nickson C. (2020). Acute traumatic spinal cord injury. Life in the Fast Lane. Retrieved from https://litfl.com/acute-traumatic-spinal-cord-injury/
Pickens, A. (2018). EM in 5: Shock. EMDocs. Retrieved from http://www.emdocs.net/em-in-5-shock/
Richards JB & Wilcox SR. (2014). Diagnosis and management of shock in the emergency department. EB Medicine, 16(3), 1-24. Retrieved from https://www.cmua.nl/Cmua/Inwerken_files/0314%20Shock.pdf

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Question Of The Day #50

August 13, 2021June 19, 2021 ~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

Explanation

This patient presents to the Emergency Department with altered mental status. This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more. The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination. One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”. The table below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient arrives hyperthermic, tachycardic in atrial fibrillation, diaphoretic, and altered with psychotic behavior. Thyroid storm, the most severe manifestation of hyperthyroidism, should always be on the differential diagnosis in patients with fever and altered mental status. Other considerations are sepsis, sympathomimetic overdose, anticholinergic overdose, serotonin syndrome, and pheochromocytoma.

This patient has thyroid storm, a life-threatening endocrine emergency that requires prompt recognition and treatment. Symptoms of thyroid storm include altered mental status, psychosis, seizures, coma, tachycardia, atrial fibrillation, high-output heart failure, dyspnea, vomiting, diarrhea, weight loss, and anterior neck enlargement. Severe hyperthyroidism should have a low-undetectable TSH level with elevated T3/T4 levels, but in acute illness these levels may be unreliable. For this reason, the diagnosis and treatment of thyroid storm should be based on clinical grounds.

An anticholinergic toxidrome can appear similar to this patient with tachycardia, hypertension, agitation, and altered mental status. A key differentiating factor is diaphoresis. Patients with anticholinergic ingestions should have dry skin, not wet skin. The treatment for anticholinergic toxicity is benzodiazepines and IV physostigmine (Choice A) if symptoms are unresponsive to benzodiazepines. Physostigmine is not the best next step in this scenario.

Treatment of thyroid storm is algorithmic. First, beta blockade (Choice C) should be given to control the heart rate and block T4 to T3 conversion, next anti-thyroid medications (Methimazole or Propylthiouracil (Choice D)) should be given to block thyroid hormone synthesis, and lastly corticosteroids and inorganic iodine (Choice B) can be given to block release of stored thyroid hormone. The best next step in managing this patient with thyroid storm is administration of IV Propranolol (Choice C). Propranolol helps manage the tachycardia, systemic symptoms, and also inhibits conversion of T4 to T3.

Correct Answer: C

References

Alvarez, A & Sekhon, N. (2019). Altered Mental Status. Society of Academic Emergency Medicine. Retrieved from https://www.saem.org/cdem/education/online-education/m4-curriculum/group-m4-approach-to/approach-to-altered-mental-status
Lee, T. (2013). Diagnosing hyperthyroidism: Answers to 7 common questions. ALiEM. Retrieved from https://www.aliem.com/diagnosing-hyperthyroidism/
Swaminathan, A. (2017). Thyroid Storm. CORE-EM. Retrieved from https://coreem.net/core/thyroid-storm/

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Question Of The Day #49

August 6, 2021June 19, 2021 ~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most likely cause of this patient’s condition?

Explanation

ALTERED MENTAL STATUS

Hyperthermia (or hypothermia) can cause altered mental status. This patient arrives with altered mental status, severe hyperthermia, tachycardia, tachypnea, and hypotension. The history of the patient running outside for exercise should raise concern for hyperthermia related to excess heat production due to overexertion. This should narrow the differential diagnoses to heat exhaustion (Choice B) and heat stroke (Choice C). Both heat exhaustion and heat stroke are marked by hyperthermia with temperatures often over 40ᵒC. Additional symptoms include weakness, nausea, vomiting, myalgias, syncope, and headache. The differentiating factor between heat exhaustion and heat stroke is altered mental status and sweating. Patients with heat exhaustion lack altered mental status and should still be able to thermoregulate through sweating. On the contrary, heat stroke patients are more severely ill as they have altered mental status and can no longer thermoregulate with sweating. The treatment in both conditions should be early and aggressive cooling measures. This includes full body immersion in an ice bath, removal of clothes, and cold IV fluids. Internal cooling with gastric, bladder, pleural, or peritoneal lavage with cold fluids can be done on more sick patients. Antipyretic medications, like NSAIDs and paracetamol, have no benefit in patients with severe hyperthermia. Evaluation for rhabdomyolysis, kidney failure, liver failure, sepsis, or other organ dysfunction should also be a part of the evaluation of hyperthermic patients.

Sympathomimetic toxicity (Choice A) is possible, but less likely as the skin is dry and the history of exercise outdoors. Sympathomimetic toxicity manifests as diaphoresis, tachycardia, hypertension, hyperthermia, and sometimes altered mental status. Thyroid storm (Choice D) is another possibility. This diagnosis can also present with similar vital signs, hyperthermia, and altered mental status. Again, the history of outdoor exercise should point more towards heat exhaustion vs heat stroke.

The diagnosis of this patient is heat stroke (Choice C) as he has altered mental status and lacks wet skin.

Correct Answer: C

References

Alvarez, A & Sekhon, N. (2019). Altered Mental Status. Society of Academic Emergency Medicine. Retrieved from https://www.saem.org/cdem/education/online-education/m4-curriculum/group-m4-approach-to/approach-to-altered-mental-status
Nickson, C. (2020). Hyperthermia. Life in the Fast Lane. Retrieved from https://litfl.com/hyperthermia/
Swaminathan, A. (2017). Environmental hyperthermia. CORE-EM. Retrieved from https://coreem.net/core/environmental-hyperthermia/

[cite]

Cerebral Venous Sinus Thrombosis

August 2, 2021June 20, 2021 ~ Sumaiya Hafiz, UAE ~ Leave a comment

One of the most frequent presentations in the ED is a patient complaining of headache. There is a wide range of differentials, such as mental illnesses to life threatening causes. Cavernous sinus thrombosis is amongst them, thus making it one of the main causes that need to be ruled in or out when a patient first presents to the ED with complaints of headache.

The most common presentation you may encounter or a presentation frequently asked in exams would be of a young female on oral contraceptive pills who presents with a headache and limb weakness. Although the list of differentials is long, cerebral venous thrombosis should definitely be kept amongst the top 3, as early diagnosis is key.

What is Cerebral Venous Thrombosis (CVT)?

CVT is the formation of a clot in the cerebral veins and the dural sinuses. The dural sinuses consist of the superior sagittal sinus, straight sinus, and transverse sinus. These are the sites commonly affected by clot formation. Rarely, it may present in cortical veins and jugular veins.

It is considered a type of stroke and is divided into three types: acute, subacute, and chronic.

Epidemiology and Risk Factors

Young patients between the ages of 20-50 years are most commonly affected, especially women of the age group are affected more compared to men.

People with factors contributing to Virchow’s Triad (stasis, endothelial injury, and hypercoagulability) are at a higher risk of getting affected. Other factors include – genetic disorders such as thrombophilia, APS – antiphospholipid syndrome, autoimmune disorders, malignancies, pregnant women, recent surgery, use of oral contraceptive pills, infections (most commonly sinusitis and meningitis), patients who recently underwent lumbar puncture, and catheterization of the jugular vein.

Anatomy

Cerebral veins are compromised of a deep and superficial system. The veins do not have valves. There are several connections between the veins of both systems and the sinuses.

Venous blood from cerebral veins drains into the major dural sinuses and the internal jugular vein. The superficial system mainly drains into the superior sagittal sinus and the lateral sinus.

Pathophysiology

How does it happen? The exact mechanism is unknown; however several studies propose the following theory: Thrombus formation in veins causes obstruction as the blood pools and raises pressure within the blood vessels and decreases CSF drainage. This CSF collection gives rise to intracranial hypertension and hydrocephalus, leading to the most common symptom patients present with – headache and stroke-like symptoms. Almost half of the cases have hemorrhagic transformation prior to treatment.

History and Physical Examination

The presentation is non-specific and may mimic other illnesses, making it one of the hardest to diagnose.

The history and physical examination findings depend on the extent of the thrombosis.

Some of the most common complaints in patients with CVT include-

Headache is the most common presentation – in the case of a patient complaining of sudden onset headache typical of subarachnoid hemorrhage, CVT should always be kept in mind as an uncommon yet possible cause.
Nausea, vomiting may also be present.
Seizures
Papilledema
Focal neurological deficits – weakness, gait, and visual abnormalities have all been reported
If the thrombosis extends to the jugular vein, there will be signs of multiple cranial nerve involvement :

Lesions in the superior sagittal sinus can present with seizures and motor dysfunction

Lesions in the left transverse sinus may cause patients to be aphasic

Lesions in the cavernous sinus could present with periorbital pain and visual changes

Lesions in deep venous sinuses may present with altered mental status

Differentials

Infections – meningitis, encephalitis
Trauma
Benign intracranial hypertension
6th Cranial Nerve Palsy
Stroke
Cavernous sinus thrombosis

Investigations and Imaging

Full blood count – increased hemoglobin due to polycythemia, decreased platelet count, and increased white blood cell count are all important factors
In patients suspected to have hereditary hypercoagulable states, appropriate diagnostic tests may be done such as protein c and S deficiency, antiphospholipid syndrome, factor V Leiden
Lumbar puncture may be done if meningitis or encephalitis is suspected to be the cause
D-dimer level

Various imaging modalities are used to diagnose CVT, or the conditions leading to it.

CT Scan- hyperdensity in the lumen- dense clot sign & Empty delta sign (filling defect in the dural sinus)
CT Angio
MRI
Magnetic Resonance Venogram (MRV)- Gold standard

1) Empty delta sign

2) Dense clot sign

3) MRV of the Cerebral Venous System (Saposnik 2011)

Treatment and Management

t is important to treat CVT, including its cause and complications. CVT treatment is quite similar to the treatment of stroke with the use of thrombolysis and anticoagulation. The treatment modalities have been controversial due to the risk of bleeding, but several studies conducted showed a much greater benefit of anticoagulation and thrombolysis in patients with CVT. Parenteral administration of Heparin or the use of Enoxaparin is preferred in the acute phase.

In patients who do not improve by anticoagulation treatment, thrombolytics are administered systemically or catheter directed. Common thrombolytics used are Tenecteplase and alteplase. After acute management, patients are prescribed warfarin for 3-6 months duration.

Treating the cause includes appropriate antibiotic coverage for infections, methods of lowering intracranial pressure, anticonvulsants for seizure control and care must be taken to prevent aspiration in patients with focal neurological deficits.

Prognosis

Death due to herniation is common, and decompressive surgery to prevent this has greatly reduced morbidity and mortality. The mortality associated with CVT is 5%.

Things To Consider

As the emergency physicians are the first ones to evaluate the patient, any patient who presents with stroke-like symptoms, headache – especially first occurrence and extremely painful, with a significant history of blood disorders or oral contraceptive use, CVT should be considered, and the appropriate tests must be ordered in order to make a timely diagnosis and begin management to prevent morbidity and mortality.

References and Further Reading

Cerebral venous thrombosis – WikEM. (2021). https://wikem.org/wiki/Cerebral_venous_thrombosisCerebral Venous Thrombosis: Background, Etiology, Epidemiology. (2021). https://emedicine.medscape.com/article/1162804-overview
https://www.med.umich.edu/1libr/Stroke/SinusVeinThrombosis.pdf
Idiculla P, S, Gurala D, Palanisamy M, Vijayakumar R, Dhandapani S, Nagarajan E: Cerebral Venous Thrombosis: A Comprehensive Review. Eur Neurol 2020;83:369-379. doi: 10.1159/000509802
Nickson, C. (2021). Cerebral Venous Thrombosis • LITFL • CCC Neurology https://litfl.com/cerebral-venous-thrombosis/

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Recent Blog Posts By Sumaiya Hafiz

Under the scorching sun – Heat Stroke Q&A

Cerebral Venous Sinus Thrombosis

Intern Survival Guide – ER Edition

Dermatological emergencies : Stevens-Johnson Syndrome

Hypokalemic Periodic Paralysis in the ED

Triads in Medicine – Rapid Review for Medical Students

Question Of The Day #48

July 30, 2021June 19, 2021 ~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most likely cause of this patient’s condition?

Explanation

ALTERED MENTAL STATUS

The first step in managing this patient should be to treat the hypoxia with supplemental oxygen. Prolonged hypoxia is dangerous and if left untreated, can cause brain damage. Hypoxia can cause altered mental status, however, when this patient’s hypoxia is resolved, she remains somnolent and altered. This should raise concern over an alternative etiology for the patient’s condition.

The arterial blood gas demonstrates a low pH (acidosis), normal paO2, elevated paCO2 (hypercarbia), and a normal HCO3 (no metabolic compensation for acidosis). The final interpretation of the ABG would be an acute respiratory acidosis without metabolic compensation. Acute elevations of pCO2 can manifest as somnolence and altered mental status as seen in this patient. This is known as hypercarbic or hypercapnic respiratory failure (Choice A). This condition is caused by the inability to exhale CO2. Risk factors include obstructive lung diseases (i.e., COPD), obesity, and obstructive sleep apnea. Treatment involves treatment of hypoxia with supplemental oxygen, non-invasive positive pressure ventilation (i.e., BIPAP, CPAP, High Flow Nasal Cannula), and treatment of the underlying cause.

The patient’s arterial blood gas does not show hypoxic respiratory failure (Choice B). Since treatment of the patient’s hypoxia does not improve the patient’s mental status, hypercarbic respiratory failure is more likely the underlying cause of the patient’s condition. Opioid overdose (Choice C) can cause a similar ABG and patient presentation. The normal size pupils and absent history of drug abuse makes this diagnosis less likely. Sepsis (Choice D) can trigger changes in mental status and cause respiratory failure, however, the absence of infectious symptoms and the presence of obesity and COPD support hypercarbic respiratory failure as the more likely underlying cause.

Correct Answer: A

References

Alvarez, A & Sekhon, N. (2019). Altered Mental Status. Society of Academic Emergency Medicine. Retrieved from https://www.saem.org/cdem/education/online-education/m4-curriculum/group-m4-approach-to/approach-to-altered-mental-status
Cadogan, M. (2020). Acid base disorders. Life in the Fast Lane. Retrieved from https://litfl.com/acid-base-disorders/
Farkas, J. (2017). PulmCrit – Optimizing the respiratory drive to avoid failure. PulmCrit. Retrieved from https://emcrit.org/pulmcrit/respiratory-drive/

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Question Of The Day #47

July 23, 2021June 19, 2021 ~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

Explanation

ALTERED MENTAL STATUS

The initial approach to all Emergency Department patients, especially those with abnormal vital signs, should include a primary survey (“ABCs”, or Airway, Breathing, Circulation). This patient is breathing independently but at a significantly reduced rate and is hypoxic. Hypoxia should prompt the administration of supplemental oxygen to the patient and reassessment of the SpO2. The patient’s reduced respiratory rate, lethargy, and bilateral miosis (constricted pupils) should strongly hint at the possibility of opioid overdose. Although the patient is lethargic and hypoxic, establishing a definitive airway (endotracheal intubation) should be avoided until after the antidote to opioid overdose is administered. Naloxone is a mu-opioid receptor antagonist and functions as the antidote to opioid overdose.

Administration of 1000mL of 0.9% NaCl (Choice A) is unlikely to fix the patient’s clinical condition. The patient needs naloxone to improve respiratory status. 25g of IV dextrose (Choice B) would be helpful if this patient’s altered mental status was from hypoglycemia. A normal glucose level is provided in the question stem. 100mg of IV thiamine (Choice D) may be helpful in the case of Wernicke-Korsakoff Syndrome, a state of thiamine deficiency often associated with malnutrition and alcohol abuse. Wernicke-Korsakoff Syndrome presents with vision disturbances, ataxia, and confusion. Typically, this syndrome does not present with severe lethargy or depressed mental status as is seen in this patient.

The best next step in management is 1mg of IV naloxone (Choice C). If given appropriately, naloxone can prevent the need for intubation. Naloxone has a very short onset to action (~1min). If suspicion for opioid overdose is high and there is an inadequate respiratory response after a single naloxone dose, repeat doses of naloxone are appropriate. Naloxone can be administered in repeat boluses every 3-minutes to a total dose of 10mg IV. Patients who respond appropriately to naloxone should be observed for recurrent respiratory depression as naloxone is cleared. Need for repeat doses of naloxone indicates the need for a continuous naloxone infusion and hospital admission. The typical infusion dose is 2/3 the “wake-up” dose given over 1 hour as a continuous infusion. For example, if the patient responded to 1mg IV initially, the continuous infusion dose would be 0.6mg/hour of IV naloxone.

Correct Answer: C

References

Alvarez, A & Sekhon, N. (2019). Altered Mental Status. Society of Academic Emergency Medicine. Retrieved from https://www.saem.org/cdem/education/online-education/m4-curriculum/group-m4-approach-to/approach-to-altered-mental-status
Nickson, C. (2020). Opioid overdose. Life in the Fast Lane. Retrieved from https://litfl.com/opioid-overdose/

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Question Of The Day #46

July 16, 2021June 19, 2021 ~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

Explanation

ALTERED MENTAL STATUS

The serum chemistry results provided show elevated BUN and Creatinine with a BUN/Cr ratio of 21.3. A BUN/Cr ratio greater than 20 indicates decreased perfusion to the kidneys, also known as pre-renal azotemia, which can indicate dehydration, hypovolemia, or shock. The serum chemistry also shows a severely low sodium level. Hyponatremia can present with a variety of symptoms, including weakness, fatigue, myalgias, nausea, vomiting, headaches, altered mental status, focal neurologic deficits, seizures, or coma. Hyponatremia can be acute or chronic, asymptomatic or symptomatic, and mild or severe. Sodium levels below 120 mEq/L are severely low. Neurologic symptoms, such as seizures, altered mental status, and focal neurologic deficits, are also considered severe. Treatment should be based on patient symptoms, rather than the sodium level, as it can be difficult to assess how acute or chronic the hyponatremia state is on initial evaluation. The presence of any severe neurologic symptoms as is seen in this scenario should prompt administration of hypertonic saline (3% NaCl). This allows for rapid correction of serum sodium levels, which should in turn relieve the neurologic symptoms. A 100-150mL IV bolus of 3% NaCl can be given a second time if symptoms continue after 5-10 minutes.

Typically, hyponatremia should be corrected slowly to avoid central pontine myelinolysis. Increases in sodium greater than 8mEq/L per 24hours should be avoided for this reason. However, in the case of neurologic symptoms, rapid correction of sodium is opted for to prevent further damage.

Administration of “normal saline”, or 1000mL of IV 0.9% NaCl (Choice A), can increase the sodium level. However, normal saline is not concentrated enough to rapidly increase the serum sodium to terminate neurologic symptoms. A noncontrast CT scan of the head (Choice B) is a reasonable investigation for this altered patient, but hypertonic saline should be administered first if hyponatremia is known. Administration of 25mg IV dextrose (Choice C), also known as “D50”, would be helpful in a patient with hypoglycemia and altered mental status. However, this patient is not hypoglycemic.

Administration of hypertonic saline (Choice D) is the best next step in this patient with severe hyponatremia and neurologic symptoms.

Correct Answer: D

References

Alvarez, A & Sekhon, N. (2019). Altered Mental Status. Society of Academic Emergency Medicine. Retrieved from https://www.saem.org/cdem/education/online-education/m4-curriculum/group-m4-approach-to/approach-to-altered-mental-statu
Farkas, J. (2020). Hyperosmolar hyperglycemic state (HHS). EMCRIT: The Internet Book of Critical Care. Retrieved from https://emcrit.org/ibcc/hhs/
MDCalc. Sodium Correction for Hyperglycemia. Retrieved from https://www.mdcalc.com/sodium-correction-hyperglycemia#evidence

[cite]

Question Of The Day #45

July 9, 2021June 19, 2021 ~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

Explanation

ALTERED MENTAL STATUS

This patient’s altered mental status is likely due to a post-ictal state after a first-time seizure. A seizure occurs when the brain is in a state of neuronal hyperactivity. First time seizures can be caused by a variety of factors, such as hypoxia, hyperthermia, hypoglycemia, traumatic brain injury, brain tumors, meningitis, encephalitis, hyponatremia, or alcohol withdrawal. It can sometimes be difficult to differentiate a seizure from a syncopal episode. Both conditions cause loss of consciousness and both may include body convulsions. Details that support a diagnosis of seizure over syncope include bowel or bowel incontinence, tongue biting, and confusion after regaining consciousness (post-ictal state).

Management of a patient having a seizure should focus initially on the ABCs (Airway-Breathing-Circulation) and terminating the seizure. This involves first repositioning the patient to prevent aspiration. A common maneuver is rolling the patient in the lateral decubitus position, performing a jaw thrust, and suctioning the airway (Choice C). Administration of IM haloperidol (Choice A) is unlikely to terminate the seizure as it is an antipsychotic, not an antiepileptic medication. Obtaining a 12-lead EKG (Choice D) is an important aspect of evaluating a patient with a potential seizure, however, the next best step in this seizing patient should focus on the ABCs and terminating the seizure. Endotracheal intubation (Choice B) may be necessary in this patient to protect the airway, but patient repositioning (Choice C) and antiepileptic (i.e., benzodiazepines) administration are important initial steps prior to considering intubation. The best next step in this scenario is Choice C.

Correct Answer: C

References

Alvarez, A & Sekhon, N. (2019). Altered Mental Status. Society of Academic Emergency Medicine. Retrieved from https://www.saem.org/cdem/education/online-education/m4-curriculum/group-m4-approach-to/approach-to-altered-mental-status
Nickson, C. (2020). Status epilepticus. Life in the Fast Lane. Retrieved from https://litfl.com/status-epilepticus/
White, R. (2017). Approach to adult first time seizure in the ED. CORE-EM. Retrieved from https://coreem.net/core/1st-time-seizure/

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You have a new patient!

What do you need to know?

Primary Headache Disorders

Migraine

Cluster Headache

Tension Headache

Secondary Headache Disorders

Subarachnoid Hemorrhage (SAH)

Intracranial Neoplasms

Meningitis

Giant Cell Arteritis (GCA, or Temporal arteritis)

Carotid and Vertebral Artery Dissection

Cerebral Vein Thrombosis (CVT)

Initial Assessment and Stabilization (ABCDE approach)

Medical History

Physical Examination

When To Ask Your Senior for Help

Not-To-Miss Diagnoses

Acing Diagnostic Testing

Empiric and Symptomatic Treatment

Procedures

Lumbar Puncture [14]

Special Patient Groups

Pregnant Patients

Children

Elderly

When To Admit

Revisiting Our Patient

Author

Shailaja Sampangi Ramaiah

Listen to the chapter

References

Reviewed and Edited By

Joseph Ciano, DO, MPH, MS

Arif Alper Cevik, MD, FEMAT, FIFEM

Sharing is caring

Like this:

You have a new patient!

What do you need to know?

Importance

Epidemiology

Pathophysiology

Table 1: Common Infectious Causes of Meningitis [7-14].

Medical History

Physical Examination

Table 2: Common signs/symptoms of meningitis, with sensitivity [8-10]

Alternative & Differential Diagnoses

Acing Diagnostic Testing

Table 3: CSF Testing Characteristics [9-11, 17-19]

Risk Stratification

Management

Special Patient Groups

When To Admit This Patient

Revisiting Your Patient

Author

J. Austin Lee, MD MPH DTMH

Listen to the chapter

References

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Sharing is caring

Like this:

You have a new patient!

What do you need to know?

Importance

Epidemiology & Pathophysiology

Medical History

Table 1: Key symptoms to look for to differentiate between delirium and dementia during history taking [11]

Typical presentations of dementia of various type

Physical Examination

Table 2: Key signs to look for to differentiate between delirium and dementia during physical exam [11]

Alternative Diagnoses

Table 3: Alternative diagnoses of altered cognitive level [14]

Acing Diagnostic Testing

Initial Investigations

Further Investigations If A Differential Is Suspected

Risk Stratification

Table 4: Abbreviated mental test score four-item version (AMT4)

Management

Special Patient Groups