Carbon Monoxide Poisoning (2024)

November 29, 2024December 2, 2024 ~ iEM Education Project Team ~ Leave a comment

by Mohammad Issa Naser & Abdulla Alhmoudi

You have a new patient!

A 48-year-old male with a known medical history of hypertension, depression, and prior suicidal attempts was brought into the Emergency Department by EMS after he was found unconscious by his wife after she arrived from work. He was lying down in an enclosed garage at home with the car engine running. She states that her husband was having difficulty breathing when she found him and was not responding to her. She reported that he had been depressed for the last few weeks because of financial problems. Upon arrival at the ED, the patient was unresponsive, with the following vital signs noted: BP 113/74 mmHg, HR 114 bpm, RR 10 bpm, and oxygen saturation at 98%.

What do you need to know?

Importance and Epidemiology

Carbon Monoxide (CO) is often called the “silent killer” as it lacks any warning or alarming signs of its presence. It is a colorless, odorless, tasteless, and non-irritating gas formed by the incomplete combustion of hydrocarbon fuels.

Despite a historical decline in the number of cases, CO continues to be one of the major causes of poisoning-related ED visits, accounting for approximately 50,000 cases every year in the United States, with a mortality rate of 1% to 3% [1]. Although many of these are nonfatal exposures with various degrees of toxicity, an estimated 1,000 to 2,000 patients a year die from severe toxicity [2]. Intentional poisoning cases have higher mortality rates compared to accidental cases and account for two-thirds of deaths [3,4]. Although cases can occur around the year, CO poisoning has a seasonal and geographic relation with cold climates, peaking during winter months, most commonly from faulty furnaces [5].

CO poisoning often has nonspecific toxicologic presentations ranging from minimal symptoms to unresponsiveness. It requires higher suspicion from clinicians to recognize, diagnose, and provide timely and appropriate management to avoid morbidity, mortality, and long-lasting complications. ED physicians should always consider CO poisoning when multiple patients present to the ED from a single location with similar correlating findings [3].

Pathophysiology

CO poisoning causes tissue hypoxia by impairing oxygen delivery and utilization and generating reactive oxygen species. CO can rapidly diffuse into the pulmonary circulation and reversibly bind the iron moiety of heme with approximately 240 times the affinity of oxygen-forming carboxyhemoglobin (COHb). CO impairs heme’s ability to deliver oxygen by directly occupying oxygen-binding sites and causing a conformational change to the other three oxygen-binding sites. This allosteric change increases the affinity of the oxygen binding site and decreases the oxygen delivery to the peripheral tissues, causing a leftward shift in the oxyhemoglobin dissociation curve. The amount of carboxyhemoglobin formed depends on the amount of CO and oxygen in the environment, duration of exposure, and minute ventilation [6].

CO also binds to myoglobin and NADPH reductase, which can worsen the hypoxia of cardiac muscle by affecting the mitochondria and ATP production, potentially leading to atraumatic rhabdomyolysis [2]. Like cyanide, CO inactivates cytochrome oxidase, which is involved in mitochondrial oxidative phosphorylation, causing a switch to anaerobic metabolism, and their combined effects can be synergistic in smoke inhalation [7]. Other effects of CO poisoning include neutrophil degranulation, free radical formation, lipid peroxidation in the brain and other tissues, and cellular apoptosis [2,8]. The half-life of COHb is about 300 minutes; thus, it begins to accumulate in the blood within a short exposure time. With normobaric oxygen (NBO) therapy (which is 100% inhaled oxygen at normal atmospheric pressure), the half-life is decreased to between 50 and 100 minutes; with Hyperbaric oxygen therapy, the half-life can be reduced to 30 minutes [9,10].

Medical History

A thorough history can be very helpful for early recognition of CO-related poisoning. Clinical findings can be variable and highly unspecific. The most common complaint in patients with mild to moderate CO poisoning is headache, present in up to 58% of patients, followed by the wide range of unspecific findings of nausea, dizziness, drowsiness, vomiting, cough or choking, confusion, shortness of breath, syncope, throat and eye irritation and chest pain [3]. It is important for clinicians to inquire about potential CO sources such as residential heating systems, gas appliances, or recent fires. In addition, clinicians should specifically inquire about transient loss of consciousness, as the presence or absence of this finding can be important in determining the severity of the presentation and the need for further interventions like hyperbaric oxygen [6]. Delayed neurological sequelae (DNS) is a well-known complication and can occur in 15 to 40 percent of patients presenting with significant CO poisoning [11]. DNS has been reported to appear 3 to 240 days after apparent recovery, with the majority of cases occurring within 20 days of CO poisoning. Deficits can last a year or more and are typically not found on acute presentation. Patients may present with cognitive impairment, memory deficits, movement disorders, or psychiatric symptoms. Any neurological or neuropsychiatric symptoms persisting beyond the acute phase of CO poisoning should raise suspicion for DNS and warrant appropriate evaluation and management [6]. Risk factors that predict the development of delayed neurologic sequelae include extremes of age and loss of consciousness. Because most CO-poisoned patients reaching the ED survive with minimal intervention, prevention of delayed neurologic and neuropsychiatric sequelae is a primary goal of therapy [12].

Physical Examination

Physical examination in suspected CO poisoning patients should focus on vital signs, cardiac and pulmonary examination, and a thorough neurological assessment. Findings in CO poisoning are usually limited to changes in mental status, tachycardia, and tachypnea in the absence of history of trauma or burns. Symptoms can range from mild confusion to coma [6]. The presence of “cherry-red” skin or mucous membranes may be observed in severe cases or even noted postmortem. However, it’s neither a sensitive nor specific sign, and it does not exclude CO poisoning [13]. Severe CO poisoning can be associated with neurologic, metabolic, and cardiovascular red flags such as seizures, syncope, lactic acidosis, acute myocardial infarction, ventricular arrhythmia, and pulmonary edema [6].

Alternative Diagnoses

Carbon monoxide poisoning can be a “great mimic,” but the early presentations are often nonspecific and readily confused with other conditions, typically a viral syndrome, explaining why influenza is the most common misdiagnosis [14]. CO poisoning can also be misdiagnosed frequently as gastroenteritis, food poisoning, or even colic in infants. Like adults, children tend to develop nonspecific symptoms that complicate the diagnosis [15]. More severe poisoning may be confused with other causes of altered mental status, such as trauma, diabetic ketoacidosis, meningitis, hypoglycemia, and intoxication [16]. The differential diagnosis remains broad without a known exposure source or sick contacts as clues. Cyanide poisoning, especially in patients with smoke inhalation, should also be considered due to the potential for concurrent exposure. In cases of chronic CO exposure, chronic fatigue, mood disorders, sleep disorders, and memory problems should be considered as an alternate diagnosis [17]. Recognizing risk factors for CO poisoning can be crucial in determining the likelihood of CO poisoning; focusing on potential sources of CO poisoning, the presence of multiple individuals with similar symptoms from the same location increases the likelihood of CO poisoning. The CNS is the organ system most sensitive to CO poisoning. Acutely, otherwise healthy patients may manifest headache, dizziness, and ataxia at COHb level as low as 15% to 20%; with higher levels and longer exposures, syncope, seizures, or coma may result [15]. At the same time, history of consuming contaminated food or recent sick contact with flu-like symptoms would make the diagnosis less likely.

Acing Diagnostic Testing

The single most useful diagnostic test to use in a suspected CO poisoning is COHb levels.15 An arterial or venous blood gas analysis with elevated carboxyhemoglobin levels (usually ≥ 3%-4% for nonsmokers or ≥ 10% for smokers) confirms the diagnosis of CO poisoning and provides information about lactate levels and any concurrent metabolic acidosis. It is important to obtain lactate levels to screen for possible concurrent cyanide toxicity (Lactate > 10 mmol/L) if the source of CO was a fire [18]. While an abnormally elevated COHb level indicates CO poisoning, it is important to note that the COHb levels do not accurately represent the severity of the poisoning. This is particularly true if there has been a significant time lapse between the exposure and when the levels were obtained due to CO clearance. Patients with major symptoms such as loss of consciousness altered mental status, or cardiac ischemia should be considered as severe poisoning with any abnormally elevated COHb level. CO poisoning management should focus primarily on the patient’s signs and symptoms rather than relying solely on the COHb level to guide decision-making.

Pulse oximetry (SpO2), a non-invasive bedside test, cannot be used for screening for CO poisoning, as it doesn’t differentiate oxygenated hemoglobin and carboxyhemoglobin and may yield normal values in CO poisoning despite significant tissue hypoxia. Non-invasive CO oximeters measuring COHb and methemoglobin are available and may have a role as a screening test, but their reliability in clinical settings has been questioned [6]. The American College of Emergency Physicians recommends against using pulse CO oximetry for diagnosis of CO toxicity in patients with suspected acute CO poisoning [2].

An electrocardiogram and a measurement of cardiac enzymes should be included due to the possibility of myocardial injury in patients with moderate to severe CO poisoning looking for myocardial ischemia, infarction, or arrhythmias [2,19]. Imaging studies, such as chest radiographs, may be indicated in certain clinical scenarios and can help patients presenting with hypoxia and dyspnea to evaluate for pulmonary edema [20].

Risk Stratification

Significant neurologic manifestations of CO poisoning include findings such as syncope, coma, seizures, altered mental status (GCS <15) or confusion, and abnormal cerebellar function. Metabolic findings such as lactic acidosis may be profound from cellular hypoxia. Cardiovascular findings include acute myocardial ischemia, myocardial injury, ventricular arrhythmia, and pulmonary edema [6].

The clinical policy from the American College of Emergency Physicians concerning the evaluation and management of adult patients with acute carbon monoxide poisoning presents evidence-based recommendations addressing three key clinical questions: the diagnostic accuracy of noninvasive carboxyhemoglobin measurement, the long-term neurocognitive impact of hyperbaric versus normobaric oxygen therapy, and the predictive value of cardiac testing for morbidity and mortality. The policy is based on a systematic literature review, graded using a defined class of evidence system, and offers recommendations for patient management at varying levels of certainty [21].

According to the ACEP’s CO policy, pulse CO oximetry should not be used to diagnose acute carbon monoxide (CO) poisoning due to its low sensitivity. While it offers advantages like being fast, noninvasive, and cost-effective, studies have shown it detects CO toxicity in only about 48% of cases, meaning it misses half of those affected. Similar findings were reported in other studies.

Both hyperbaric oxygen (HBO₂) and high-flow normobaric oxygen therapies are options for treating acute carbon monoxide (CO) poisoning, but it is unclear if HBO₂ is superior in improving long-term neurocognitive outcomes. While HBO₂ reduces carboxyhemoglobin levels and may aid neurologic recovery, its benefits remain debated. Meta-analyses and studies on HBO₂ have shown inconsistent results, with some finding no benefit and others suggesting improved outcomes. Variations in study designs and treatment factors contribute to the uncertainty, highlighting the need for further research.

In moderate to severe carbon monoxide (CO) poisoning, an electrocardiogram (ECG) and cardiac biomarkers should be used to detect acute myocardial injury, a predictor of poor outcomes. Studies have shown that myocardial injury is associated with higher long-term mortality and is an independent predictor of poor prognosis. Further research is needed to explore cardiac testing and interventions in less severe cases and more aggressive cardiac management for high-risk patients.

Management

Initial management starts with assessing and stabilizing the airway, breathing, and circulation. Comatose patients who have severely impaired mental status or who do not have sufficient respiratory effort should be intubated without delay and mechanically ventilated using 100 percent oxygen [6]. Treatment begins with oxygen therapy, and 100% oxygen should be provided as soon as possible with either a non-rebreather mask or endotracheal intubation, which serves two purposes. First, the half-life of COHb is inversely related to PaO2; it can be reduced from approximately 5 hours in room air to 1 hour by providing supplemental 100% oxygen. HBO therapy (at 3 atmospheres) further reduces the half-life to approximately 30 minutes [12]. Oxygen should be continued until the patient is asymptomatic and carboxyhemoglobin levels are ≤ 3%-4% in nonsmokers and ≤ 10% in smokers [2,18,19]. Evidence suggests that hyperbaric oxygen therapy helps prevent delayed neurologic sequelae in acute CO poisoning, but its efficacy decreases with delayed implementation [15]. HBO therapy can be used in patients presenting with a COHb level >25% (>15% if pregnant), unconscious at scene or hospital, reported syncope, persistent altered, mental status, coma, focal neurologic deficit, severe metabolic acidosis (pH <7.25) after empiric cyanide treatment if administered, or evidence of end-organ ischemia (e.g., ECG changes, elevated cardiac biomarkers, respiratory failure, focal neurologic deficit, or altered mental status). A thorough cardiovascular examination should be performed and should focus on signs of contributing cardiogenic shock or hypotension. Establishing IV access and cardiac monitoring are necessary as patients may need IV fluids or inotropes for resuscitation. An ECG and cardiac enzymes should also be included in the evaluation for cardiac ischemia in symptomatic patients at risk. Patients with altered mental status should have a blood glucose check to evaluate for hypoglycemia [6].

Special Patient Groups

Pediatrics

Children may present with subtle and non-specific findings compared to adults, and it is suggested that they can be more sensitive to the effects of CO due to their higher metabolic rates. Fussiness and decreased oral intake may be the only manifestations of CO toxicity. Although children may have higher levels of COHb due to their higher minute ventilation, which should make them more vulnerable to accumulating CO, the long-term outcomes appear favorable as they have lower rates of developing delayed neurological sequelae compared to adults. The diagnosis and management of CO poisoning in young children generally follow the same principles as for other age groups, with no substantial modifications in approach based on age [6].

Pregnant Patients

There is a lower threshold to using HBO therapy in pregnancy due to the greater affinity and the longer half-life of CO that is bound to fetal hemoglobin, the limited capacity to enhance placental perfusion and the direct effects of acidosis and hypoxemia on the fetus. While severe CO poisoning poses serious short- and long-term fetal risk, mild accidental exposure is likely to result in normal fetal outcomes. Because the fetal accumulation of CO is higher and its elimination slower than in the maternal circulation, hyperbaric oxygen may decrease fetal hypoxia and improve outcomes. While these findings provide valuable insights into the effects of CO poisoning and HBO therapy on pregnant patients and their fetuses, the available literature on this subject remains limited [6].

When To Admit This Patient

Hospitalization is warranted in cases where patients exhibit signs of hemodynamic instability, persistent neurologic symptoms, evidence of end-organ damage (including renal injury, rhabdomyolysis, cardiac ischemia, and pulmonary edema), or exposure to methylene chloride. Most patients who do not meet the criteria for HBO therapy and are not clinically ill can typically be managed in the emergency department; generally, patients who become asymptomatic with a carboxyhemoglobin (COHb) level < 5% may be safely discharged home. All patients exposed to CO require close follow-up for delayed neurologic sequelae [18].

Revisiting Your Patient

Our 48-year-old male, who has a history of prior suicidal attempts, was found unconscious in his home garage with his car engine running. The past medical history and his presentation picture put him at risk for carbon monoxide poisoning, and red flags such as his altered mental state and the recognition of a source of carbon monoxide should guide the clinician through the diagnosis and management process. Management started by assessing the airway, breathing, and circulation. The patient was in a state of respiratory arrest and was intubated and ventilated with 100% oxygen. His pupils were dilated and sluggish. The patient was hypotensive, and IV fluids were started while vasopressors were being prepared. A CBC, chemistry, blood glucose, cardiac enzymes, COHb level, and venous blood gas were requested. A Chest XR was also done, which showed no signs of pulmonary edema, and an endotracheal tube was confirmed in place. ECG showed normal sinus rhythm with no ST-T wave changes. COHb level was 38%, blood glucose 139 mg/dl, and cardiac enzymes were within normal range. His blood gas showed a pH of 7.28 and a lactate of 4. A diagnosis of carbon monoxide poisoning was made. The patient was kept on 100% oxygen and was being prepared to be transferred into a hyperbaric oxygen therapy facility.

Authors

Mohammad Issa Naser

Dr Mohammad Naser is currently a Critical Care Medicine Fellow in Sheikh Shakhbout Medical City - Abu Dhabi. He completed his emergency medicine training at Zayed Military Hospital and has obtained both the Emirati and Arab board certifications in Emergency Medicine. Dr. Naser has a profound interest in critical care medicine, particularly in bridging the gap between emergency and intensive care practices. Beyond critical care, He is deeply passionate about medical education, mentoring future healthcare professionals, and developing innovative teaching tools. Additionally, he is actively involved in clinical research, focusing on advancing knowledge and practices in emergency and critical care medicine.

Abdulla Alhmoudi

Dr Abdulla Alhmoudi is a Consultant Emergency Medicine, serving at Zayed Military Hospital and Sheikh Shakhbout Medical City - Abu Dhabi. He pursued his residency training in Emergency Medicine at George Washington University in Washington DC and further enhanced his expertise with a Fellowship in Extreme Environmental Medicine. Dr Alhmoudi's passion for medical education is evident in his professional pursuits. He currently holds the position of Associate Program Director at ZMH EM program and is a lecturer at Khalifa University College of Medicine and Health Sciences. Beyond medical education, he maintains a keen interest in military medicine and wilderness medicine.

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References

Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy [published correction appears in Am J Respir Crit Care Med. 2017 Aug 1;196 (3):398-399]. Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Carbon Monoxide Poisoning:, Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Carbon Monoxide Poisoning. Ann Emerg Med. 2017;69(1):98-107.e6. doi:10.1016/j.annemergmed.2016.11.003
Shin M, Bronstein AC, Glidden E, et al. Morbidity and Mortality of Unintentional Carbon Monoxide Poisoning: United States 2005 to 2018. Ann Emerg Med. 2023;81(3):309-317. doi:10.1016/j.annemergmed.2022.10.011
Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy [published correction appears in Am J Respir Crit Care Med. 2017 Aug 1;196 (3):398-399]. Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
Centers for Disease Control and Prevention (CDC). Unintentional non-fire-related carbon monoxide exposures–United States, 2001-2003. MMWR Morb Mortal Wkly Rep. 2005;54(2):36-39.
Manaker S, Perry H. (2023) Carbon monoxide poisoning, UpToDate. Available at: https://www.uptodate.com/contents/carbon-monoxide-poisoning (Accessed: 15 May 2023).
Norris JC, Moore SJ, Hume AS. Synergistic lethality induced by the combination of carbon monoxide and cyanide. Toxicology. 1986;40(2):121-129. doi:10.1016/0300-483x(86)90073-9
Dubrey SW, Chehab O, Ghonim S. Carbon monoxide poisoning: an ancient and frequent cause of accidental death. Br J Hosp Med (Lond). 2015;76(3):159-162. doi:10.12968/hmed.2015.76.3.159
Weaver LK, Howe S, Hopkins R, Chan KJ. Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest. 2000;117(3):801-808. doi:10.1378/chest.117.3.801
Walker AR. Emergency department management of house fire burns and carbon monoxide poisoning in children. Curr Opin Pediatr. 1996;8(3):239-242. doi:10.1097/00008480-199606000-00009
Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy [published correction appears in Am J Respir Crit Care Med. 2017 Aug 1;196 (3):398-399].Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
Meaden CW, Nelson LS. Inhaled Toxins. In: Rosen’s Emergency Medicine Concepts and Clinical Practice. 10th ed. Elsevier; 2023:666-681.
Harper A, Croft-Baker J. Carbon monoxide poisoning: undetected by both patients and their doctors.Age Ageing. 2004;33(2):105-109. doi:10.1093/ageing/afh038
Dolan MC, Haltom TL, Barrows GH, Short CS, Ferriell KM. Carboxyhemoglobin levels in patients with flu-like symptoms. Ann Emerg Med. 1987;16(7):782-786. doi:10.1016/s0196-0644(87)80575-9
Tomaszewski, C. Carbon Monoxide. IN: Goldfrank’s toxicological emergencies. 9th ed. New York: McGraw-Hill Medical Pub. Division; c2011
Cho CH, Chiu NC, Ho CS, Peng CC. Carbon monoxide poisoning in children. Pediatr Neonatol. 2008;49(4):121-125. doi:10.1016/S1875-9572(08)60026-1
Eichhorn L, Thudium M, Jüttner B. The Diagnosis and Treatment of Carbon Monoxide Poisoning.Dtsch Arztebl Int. 2018;115(51-52):863-870. doi:10.3238/arztebl.2018.0863
Hampson NB, Piantadosi CA, Thom SR, Weaver LK. Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning.Am J Respir Crit Care Med. 2012;186(11):1095-1101. doi:10.1164/rccm.201207-1284CI
Weaver LK. Clinical practice. Carbon monoxide poisoning.N Engl J Med. 2009;360(12):1217-1225. doi:10.1056/NEJMcp0808891
Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review.J Neurol Sci. 2007;262(1-2):122-130. doi:10.1016/j.jns.2007.06.037
American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Carbon Monoxide Poisoning:, Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Carbon Monoxide Poisoning. Ann Emerg Med. 2017;69(1):98-107.e6. doi:10.1016/j.annemergmed.2016.11.003

Reviewed and Edited By

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.

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

Locker T, Mason S, Rigby A. Headache management–are we doing enough? An observational study of patients presenting with headache to the emergency department. Emerg Med J. 2004;21(3):327-332. doi:10.1136/emj.2003.012351
GBD 2015 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015 [published correction appears in Lancet. 2017 Jan 7;389(10064):e1]. Lancet. 2016;388(10053):1545-1602. doi:10.1016/S0140-6736(16)31678-6
Thomas K, Benjamin W.F, Rosen’s emergency medicine: concepts and clinical practice: St. Louis, Mosby; 2002. Chapter 93, Headache disorders; p.1265-77.
Do TP, Remmers A, Schytz HW, et al. Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology. 2019;92(3):134-144. doi:10.1212/WNL.0000000000006697
Leone, Massimo and Paola Di Fiore (2014), “Migraine and Cluster Headache.”
Millea, Paul J. and Jonathan J. Brodie (2002), “Tension-Type Headache,” American Family Physician.
Vivancos J, Gilo F, Frutos R, et al. Clinical management guidelines for subarachnoid haemorrhage. Diagnosis and treatment. Neurologia. 2014;29(6):353-370. doi:10.1016/j.nrl.2012.07.009
Alentorn, Agusti, Khê Hoang-Xuan, and Tom Mikkelsen (2016), “Presenting signs and symptoms in brain tumors.”
Siddiqui, Emaduddin (2012), “Neurologic Complications of Bacterial Meningitis.”
Smith, Jonathan H. and Jerry W. Swanson (2014), “Giant Cell Arteritis,” Headache.
Sheikh, Huma U. (2016), “Headache in Intracranial and Cervical Artery Dissections,” Current Pain and Headache Reports.
Mehta, Amit, Julius Danesh, and Deena E. Kuruvilla (2019), “Cerebral Venous Thrombosis Headache,” Current Pain and Headache Reports.
Bollero, Daniele, Maurizio Stella, Ezio Nicola Gangemi, L. Spaziante, J. Nuzzo, G. Sigaudo, and F. Enrichens (2010), “Purpura fulminans in meningococcal septicaemia in an adult: a case report,” Annals of burns and fire disasters.
Niemantsverdriet, Ellis, Hanne Struyfs, Flora H. Duits, Charlotte E. Teunissen, and Sebastiaan Engelborghs (2015), “Techniques, Contraindications, and Complications of CSF Collection Procedures.”
Gomez-Beldarrain, Marian and Juan Carlos Garcia-Monco (2014), “Lumbar Puncture and CSF Analysis and Interpretation.”
Negro A, Delaruelle Z, Ivanova TA, et al. Headache and pregnancy: a systematic review. J Headache Pain. 2017;18(1):106. Published 2017 Oct 19. doi:10.1186/s10194-017-0816-0
Raucci U, Della Vecchia N, Ossella C, et al. Management of Childhood Headache in the Emergency Department. Review of the Literature. Front Neurol. 2019;10:886. Published 2019 Aug 23. doi:10.3389/fneur.2019.00886
Reinisch, Veronika M., Christoph J. Schankin, J. Felbinger, P. Sostak, and Andreas Straube (2008), “Headache in the elderly,” Schmerz.

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

Doctor, My Head Hurts!

August 24, 2020July 25, 2020 ~ Arthur Martins, Brasil ~ Leave a comment

February was the last of my three months at Family Medicine clinical rotation. In addition to normal clinical consultations, we also had to take turns attending spontaneous demands coming “from the street”, in a primary care resource center that works similar to a green zone setting in the ED. During these three months, I’ve noticed that, sometimes, the easiest patient to manage is that one with a major complaint like chest pain, severe dyspnea, altered mental status, and so on. Things become more difficult, however, when you have a patient that has just a headache, a very common symptom, but one that could be related to an enormous variety of conditions, some of which life-threatening. Sometimes, you dig under the “green” patient and discover a secret “yellow” or even a “red” condition.

Next, I will try to put some light on the investigation of one of the most common complaints I’ve seen, and one of the symptoms that always put a bug in the ear: Headache.

Epidemiology

Headache is a very common complaint at the Emergency Department, being the fifth leading cause of ED visits¹. Alarmingly, about 0.5% of patients who had presented with a headache and discharged home have returned with a serious condition, of which 18% were acute ischemic stroke.²

Clinical Presentation

Patients can describe headache, a very nonspecific and hard to clarify complaint, in diverse ways, ranging from saying solely “my head hurts” to making a circular gesture around his/her head with. Therefore, identifying potential risk factors that can alert us to potential adverse outcomes. Here are a few decision rules for patients with headache:

SNNOOP10

The mnemonic SNNOOP10³ refers to the red flag symptom and findings to screen, which may point to related secondary headaches.

Ottawa Subarachnoid Hemorrhage Rule

Ottawa Subarachnoid Hemorrhage Rule fundamentally helps to rule out (Sensitivity: 100% Specificity: 15%) subarachnoid hemorrhage (SAH) in patients with headache. You can apply this rule ONLY IF:

The patient is alert and older than 15 years old with
New severe non-traumatic headache, reaching maximum intensity within 1 hour and
NO new neurological deficits, no history of intracranial tumors, previous SAH or aneurysms, and similar headaches (≥ 3 episodes over ≥ 6 months)

Risk factors are:

Age ≥ 40
Neck pain or stiffness
Witnessed loss of consciousness
Onset during exertion
“Thunderclap headache” (defined as instantly and immediately peaked pain)
Limited neck flexion on examination (defined as the inability to touch chin to chest or raise head 3 cm off the bed if supine)

If ANY of these factors is present, SAH can not be ruled out, and this patient needs further investigation. A recent study has assessed the performance of the Ottawa decision rule for patients presenting with headache in the ED, showing that it is a highly sensitive test (100%), making it useful in order to “not miss the disguised red patient.”⁵ Not by coincidence, Tintinalli’s book states with bold letters: “Acute onset of a severe headache is subarachnoid hemorrhage until proven otherwise.”

Acute onset of a severe headache is subarachnoid hemorrhage until proven otherwise.

Tintinalli's Comprehensive Study Guide Tweet

Investigation

Neuroimaging is a valuable diagnostic tool but is also an expensive one. Besides, it can be harmful due to radiation exposure or contrast use.

There is a lot of controversy in the literature regarding the question “When to image patients with a headache?”, but the consensus is to image when a patient presents with red flags, especially those related to vascular causes, raised intracranial pressure and focal signs.4

CT scan is the preferred method to investigate SAH, with excellent sensitivity and specificity (both bigger than 90%) in the first 6 hours of hemorrhage.6 However, if more time has passed, other diagnostic tools will probably be required in this case. Also, as said before, the costs are a major factor regarding neuroimaging, and sometimes you have to use what you have.

Lumbar Puncture

Indications⁷:
- Suspected infectious disease of the CNS
- Suspected SAH
- Suspected idiopathic intracranial hypertension – as diagnostic and treatment

Contraindications⁷:
- Coagulopathy (including anticoagulant drugs) or thrombocytopenia
- Infection at the puncture site
- Suspected epidural abscess
- Findings on the CT scan to deferring LP
- Brainstem herniation
- Mass with signs of compression of the 4th ventricle
- Signs of increased intracranial pressure or midline shift
- Acute intracranial hematoma

Disposition and Follow-up(7,8)

Most patients can be discharged with a simple painkiller prescription. About 95% of patients presenting to the ED with headache have a benign etiology and don’t need further investigation in the ED.
The acute benign headache usually resolves with acetaminophen, NSAIDs, hydration, and rest.
An adequate follow-up plan is a good practice since most headaches are due to chronic conditions that may benefit from pharmacologic prophylaxis as well as lifestyle modifications.

This subject is open to discussion. Although it looks (and it is) a simple and easy-to-manage condition 90% of times, it has the potential to give the doctor some headache, too!

References and Further Reading

American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Acute Headache:, Godwin, S. A., Cherkas, D. S., Panagos, P. D., Shih, R. D., Byyny, R., & Wolf, S. J. (2019). Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache. Annals of emergency medicine, 74(4), e41–e74. https://doi.org/10.1016/j.annemergmed.2019.07.009
Dubosh, N. M., Edlow, J. A., Goto, T., Camargo, C. A., Jr, & Hasegawa, K. (2019). Missed Serious Neurologic Conditions in Emergency Department Patients Discharged With Nonspecific Diagnoses of Headache or Back Pain. Annals of emergency medicine, 74(4), 549–561. https://doi.org/10.1016/j.annemergmed.2019.01.020
Do, T. P., Remmers, A., Schytz, H. W., Schankin, C., Nelson, S. E., Obermann, M., Hansen, J. M., Sinclair, A. J., Gantenbein, A. R., & Schoonman, G. G. (2019). Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology, 92(3), 134–144. https://doi.org/10.1212/WNL.0000000000006697
Good C. (2019). British Society Of Neuroradiologists Guidelines for Headache. Retrieved July 23, 2020, from https://bsnr.org.uk/_userfiles/pages/files/standards_and_guidelines/bsnr_guidelines_for_imaging_in_headache_april_2019_final.pdf
Wu, W. T., Pan, H. Y., Wu, K. H., Huang, Y. S., Wu, C. H., & Cheng, F. J. (2020). The Ottawa subarachnoid hemorrhage clinical decision rule for classifying emergency department headache patients. The American journal of emergency medicine, 38(2), 198–202. https://doi.org/10.1016/j.ajem.2019.02.003
Kwiatkowski T. and Friedman B. W. (2018). Headache Disorders. In: R. M. Walls, R. S. Hockberger, M. Gausche-Hill, K. Bakes, J. M. Baren, T. B. Erickson, A. S. Jagoda, A. H. Kaji, M. VanRooyen, R. D. Zane, (Eds.) Rosen’s Emergency Medicine Concepts and Clinical Practice (9th ed. pp: 1265-1277). Philadelphia, PA: Elsevier.
Perry, J. J., Stiell, I. G., Sivilotti, M. L., Bullard, M. J., Emond, M., Symington, C., Sutherland, J., Worster, A., Hohl, C., Lee, J. S., Eisenhauer, M. A., Mortensen, M., Mackey, D., Pauls, M., Lesiuk, H., & Wells, G. A. (2011). Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. British Medical Journal (Clinical research ed.), 343, d4277. https://doi.org/10.1136/bmj.d4277

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Question Of The Day #4

July 15, 2020July 12, 2020 ~ 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 describes her headache as severe, sudden-onset, and different than her prior headaches. These clues on history should raise concern for a subarachnoid hemorrhage (SAH) as the cause of her headache. Choice A (Lumbar Puncture) helps evaluate headaches caused by meningitis, pseudotumor cerebri (idiopathic intracranial hypertension), and SAH. Choice B (IV 1000mL 0.9% NaCl) is sometimes used to treat headaches, like migraines, but this patient should first receive another testing as there is a concern for SAH. Choice C (IV Ceftriaxone) is the correct initial treatment for bacterial meningitis, but this patient has a higher pretest probability for SAH. Choice D (Non-contrast CT head) is the right answer. Non-contrast CT scan of the brain performed within 6 hours of headache onset have high sensitivity to rule out aneurysmal SAH. The sensitivity of the non-contrast CT scan diminishes to 91-93% at 24hours after headache onset and continues to decrease after this to 50% sensitivity at seven days after pain onset. Lumbar puncture is recommended for a patient with a negative CT scan, high pretest probability for SAH, and presentation after 6 hours of headache onset. Findings on Lumbar Puncture that support the diagnosis of SAH include Xanthochromia (yellow appearance of the CSF due to blood breakdown) and inadequate clearing of red blood cells in the CSF between tubes 1 and 4. Treatment for SAH includes blood pressure control, seizure prophylaxis, and neurosurgical consultation, and nimodipine to prevent vasospasm and rebleeding. The Hunt and Hess scoring system can be used to predict clinical outcomes for patients with SAH. Correct Answer: D

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

Nelson AM, Mase CA, Ma O. Spontaneous Subarachnoid and Intracerebral Hemorrhage. “Chapter 166: Spontaneous Subarachnoid and Intracerebral Hemorrhage”. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill.

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Triads in Medicine – Rapid Review for Medical Students

June 12, 2020June 7, 2020 ~ Sumaiya Hafiz, UAE ~ Leave a comment

One of the most convenient ways of learning and remembering the main components of disease and identifying a medical condition on an exam are Triads, and medical students/interns/residents swear by them.

Be it a question during rounds, a multiple-choice exam question to be solved, or even in medical practice, the famous triads help physicians recall important characteristics and clinical features of a disease or treatment in an instant.

Since exam season is here, this could serve as a rapid review to recall the most common medical conditions.

While there are a vast number of triads/pentads available online, I have listed the most important (high-yy) ones that every student would be asked about at least once in the duration of their course.

1) Lethal Triad also known as The Trauma Triad of Death
Hypothermia + Coagulopathy + Metabolic Acidosis

2) Beck’s Triad of Cardiac Tamponade
Muffled heart sounds + Distended neck veins + Hypotension

3) Virchow’s Triad – Venous Thrombosis
Hypercoagulability + stasis + endothelial damage

4) Charcot’s Triad – Ascending Cholangitis
Fever with rigors + Right upper quadrant pain + Jaundice

5) Cushing’s Triad – Raised Intracranial Pressure
Bradycardia + Irregular respiration + Hypertension

6) Triad of Ruptured Abdominal Aortic Aneurysm
Severe Abdominal/Back Pain + Hypotension + Pulsatile Abdominal mass

7) Reactive Arthritis
Can’t See (Conjunctivitis) + Can’t Pee (Urethritis) + Can’t Climb a Tree (Arthritis)

8) Triad of Opioid Overdose
Pinpoint pupils + Respiratory Depression + CNS Depression

9) Hakims Triad – Normal Pressure Hydrocephalus
Gait Disturbance + Dementia + Urinary Incontinence

10) Horner’s Syndrome Triad
Ptosis + Miosis + Anydrosis

11) Mackler’s Triad – Oesophageal Perforation (Boerhaave Syndrome)
Vomiting + Lower Thoracic Pain + Subcutaneous Emphysema

12) Pheochromocytoma
Palpitations + Headache + Perspiration (Diaphoresis)

13) Leriche Syndrome
Buttock claudication + Impotence + Symmetrical Atrophy of bilateral lower extremities

14) Rigler’s Triad – Gallstone ileus
Gallstones + Pneumobilia + Small bowel obstruction

15) Whipple’s Triad – Insulinoma
Hypoglycemic attack + Low glucose + Resolving of the attack on glucose administration

16) Meniere’s Disease
Tinnitus + Vertigo + Hearing loss

17) Wernicke’s Encephalopathy- Thiamine Deficiency
Confusion + Ophthalmoplegia + Ataxia

18) Unhappy Triad – Knee Injury
Injury to Anterior Cruciate Ligament + Medial collateral ligament + Medial or Lateral Meniscus

19) Henoch Schonlein Purpura
Purpura + Abdominal pain + Joint pain

20) Meigs Syndrome
Benign ovarian tumor + pleural effusion + ascites

21) Felty’s Syndrome
Rheumatoid Arthritis + Splenomegaly + Neutropenia

22) Cauda Equina Syndrome
Low back pain + Bowel/Bladder Dysfunction + Saddle Anesthesia

23) Meningitis
Fever + Headache + Neck Stiffness

24) Wolf Parkinson White Syndrome
Delta Waves + Short PR Interval + Wide QRS Complex

25) Neurogenic Shock
Bradycardia + Hypotension + Hypothermia

Headache – A Telephone Encounter

January 20, 2020January 18, 2020 ~ Sajan Acharya, Nepal ~ Leave a comment

Learning happens in between cases in the ER. Be it a well-managed case by your colleague or a particular procedure you could have done differently. You learn something after each encounter. At times, learning happens when most unanticipated. Like when you are about to snuggle into your warm bed after a tiring day at the ER. My night was supposed to be calm, maybe punctuated by some calls by a concerned parent of minor flu ridden child, but calm nevertheless. You would not have completed rehearsing your thank you message that you are going to say the day after to the scheduler and the telephone rings. You pick it up because that is literally the only job description for tonight. Answer health queries that people might have. No wonder I was brave enough to feel cozy on the bed in the telemedicine room. It was a call from a 37-year-old female who lived in a village almost 3 hours from Patan Hospital, where I was.

At Patan Hospital, a telephone-based telemedicine service is provided 24/7 via doctors and interns working in the ED. Telephone encounter with a patient has its own challenges. For one, you don’t get to see the patient and hence won’t be able to tell the degree of discomfort. All your Sherlock Holmes like sharp power of observation that you have built through years of practice can only use one of the multiple senses. Listening becomes not only the most crucial skill but the only available tool you have.

Fear to land in the wrong place

Sometimes, you hear that one word that triggers the fast-acting, decisive and flight or fight-mode-run emergency physician in you. That forces you out of habit to think parallel while taking history. A boon and a curse in its own might, differential diagnosis starts popping up and canceling themselves. The goal is either 1) providing the patient reassurance that nothing serious is going on and she can visit a primary care in convenience or 2) urging them to visit the nearest ER because something sinister might be going on. The division seems very black and white but the near distance between the two divisions is so big that you fear to land in the wrong place without a return ticket.

Differentiating headaches

For a starting practitioner that I was, differentiating primary headaches was easier in a precisely articulated MCQ but rather difficult in a real patient scenario.

Temporally jumbled case history, intersecting symptomatology, and vital clues to the diagnosis buried underneath a mist of unrelated information constitute a patient history. To dissect through that mist and reach a sensible differential is an art that comes with practice. As I am sure I will reiterate in years to follow, I hadn’t honed the art form to the degree I have now. I present to you a telephone conversation between an intern on duty at telemedicine and a patient with a headache.

Telephone encounter

Patient

Hello! I have a bad headache.

Me

Hi, I am sorry you have a headache. Let’s talk for a bit; I will try to quickly characterize your headache and advise you on what to do next. Does that sound like a good plan?

Patient

mm hmm. I haven’t had this bad headache ever.

‘First or worst headache’ - this sounds like SAH.

Me

On a scale of 1 to 10, how bad is it?

Patient

I would say 8!

Headache severity

Me

When did it start?

Patient

Around 2 hours ago.

Me

Have you had comparable headaches or headaches on a regular basis?

Patient

Sometimes. I don’t remember.

Me

Do you remember how your headache started? Have you hurt your head?

Trying to rule out the obvious causes like trauma.

Patient

No, I came back from work. At first, I felt nauseous. Then the head gradually started throbbing. It felt like a drum was beating in my head.

At that point, I decided to open up UptoDate and look through the causes of thunderclap headache. SAH, cerebral infections, HTN crisis, Ischemic stroke, cerebral venous thrombosis – the list continued. (1)

Me

Apart from nausea, do you have any other symptoms?

Patient

I am finding it difficult to stay in bright light.

Photophobia! Could this be meningitis or migraine?

Me

Do you feel feverish?

Patient

Me

Any rash?

Patient

None that I see.

CNS infection checked off. I feared that I was asking too many questions. Had she presented to the ER, I would have managed her pain first, ruled out my differentials with history taking and sent her for appropriate investigations. The inability to accurately assess the degree of pain further adds to the limits of telephone medicine – you have to trust what you hear without having the opportunity to manage in real-time. History is essential to a proper recommendation, especially when that is the only tool you have – I thought to myself.

Me

Do you have any trouble seeing or walking?

Patient

She has been answering well, so no difficulty in speech - her neurological status seems intact.

Me

Do you have any other medical problems? Are you under any medication?

Patient

No. I just took paracetamol but it was of no use.

Me

Do you have nasal congestion or discharge?

Patient

Not now, but I had the flu a week back.

Acute sinusitis is another common cause of headache. (2) Having ruled out serious threatening causes of headache. I was relieved – this sounded like a case of the primary cause of headache, a common presentation in every ER. I needed to remember the differences between different primary headaches – a quick UpToDate search away. Maybe, telemedicine does have some pros – like searching up the internet might not have been very appropriate while talking to your patient.

Me

Where is your pain? Does the pain seem to spread to any other area?

Patient

It’s just in front of my head.

Me

Did you feel anything abnormal before the headache started?

Trying to rule out any aura

Patient

Me

Do you feel the urge to isolate yourself and not hear loud noises.

Patient

No. Not really.

Me

From my evaluation, you seem to be having a tension headache. It is not a serious condition and is the most common cause of people presenting with headaches. (3) But I would suggest you visit your nearby health center to ensure you get the right diagnosis nonetheless.

Learning is the summation of moments

Learning is the summation of moments we really understand something, those aha moments, ones that feel like an epiphany. I always knew photophobia and phonophobia occur in migraine and not in tension headache. I may even have read before that day that one of those can happen in tension headache as well. But never had I ever imagined that one day I would reassure a patient that she has a tension headache because she doesn’t have both. The nature of medicine is such that we really learn something after each encounter.

References

Schwedt TJ. Overview of thunderclap headache. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com/contents/overview-of-thunderclap-headache
Dodick D. Headache as a symptom of ominous disease. What are the warning signals?. Postgrad Med. 1997;101(5):46–50,55–6,62–4.
Jensen RH. Tension-Type Headache – The Normal and Most Prevalent Headache. Headache 2018; 58:339.

A 24-year-old woman presents with headache

May 29, 2019September 4, 2019 ~ iEM Education Project Team ~ Leave a comment

by Stacey Chamberlain

A 24-year-old woman presents with headache that began three hours prior to arrival to the ED. The patient was at rest when the headache began. The headache was not described as “thunderclap,” but it did reach maximum severity within the first 30 minutes. The headache is generalized and rated 10/10. She denies head trauma, weakness, numbness, and tingling in her extremities. She denies visual changes, changes in speech and neck pain. She has not taken anything for the headache. She does not have a family history of cerebral aneurysms or polycystic kidney disease. On physical exam, she has a normal neurologic exam and normal neck flexion.

Should you do a head CT and/or a lumbar puncture to evaluate for a sub-arachnoid hemorrhage in this patient?

Ottawa SAH Rule

Investigate if ≥1 high-risk variables present

Age ≥ 40
Neck pain or stiffness
Witnessed loss of consciousness
Onset during exertion
Thunderclap headache (instantly peaking pain)
Limited neck flexion on exam

A CDR to determine risk for sub-arachnoid hemorrhage (SAH) was derived and has been externally validated in a single study. The CDR’s purpose was to identify those at high risk for SAH and included those with acute non-traumatic headaches that reached maximal intensity within one hour and who had normal neurologic exams. Of note, the rule has many inclusion and exclusion criteria that the ED physician must be familiar with and was only derived for patients 16 years or older. The study authors note that the CDR is to identify patients with SAH; it is not an acute headache rule. In the validation study, of over 5,000 ED visits with acute headache, only 9% of those met inclusion criteria. Also, clinical gestalt again plays a role as the authors suggest not to apply the CDR to those who are ultra-high risk with a pre-test probability for SAH of > 50%.

The Ottawa SAH Rule was 100% sensitive but did not lead to reduction of testing vs. current practice. The authors state that the value of the Ottawa SAH Rule would be to standardize physician practice in order to avoid the relatively high rate of missed sub-arachnoid hemorrhages.

Case Discussion

By applying the Ottawa SAH Rule, this patient is low risk and does not require further investigation for a SAH.

[cite]

Acute Red Eye

September 14, 2018September 14, 2018 ~ iEM Education Project Team ~ Leave a comment

Today’s Headache

July 13, 2018July 13, 2018 ~ iEM Education Project Team ~ Leave a comment

In case you didn’t encounter headache today!

450 - subacute-chronic subdural haematoma

iEM Education Project Team uploads many clinical picture and videos to the Flickr and YouTube. These images are free to use in education. You can also support this global EM education initiative by providing your resources. Sharing is caring!

You have a new patient!

What do you need to know?

Importance and Epidemiology

Pathophysiology

Medical History

Physical Examination

Alternative Diagnoses

Acing Diagnostic Testing

Risk Stratification

Management

Special Patient Groups

Pediatrics

Pregnant Patients

When To Admit This Patient

Revisiting Your Patient

Authors

Mohammad Issa Naser

Abdulla Alhmoudi

Listen to the chapter

References

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

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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

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Epidemiology

Clinical Presentation

SNNOOP10

Ottawa Subarachnoid Hemorrhage Rule

Investigation

Lumbar Puncture

Disposition and Follow-up(7,8)

References and Further Reading

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Reference

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Further Reading

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Fear to land in the wrong place

Differentiating headaches

Telephone encounter