Imaging

DALLAS – On average, 22% of the CTs and MRIs ordered by emergency physicians are "medically unnecessary," based on responses by 435 emergency physicians participating in a national survey.

"The overwhelming majority of physicians in our sample recognized the issue of overimaging in the ED, and it’s not just something they felt was going on among others in their group. It’s something they personally acknowledged participating in," Dr. Hemal K. Kanzaria said at the annual meeting of the Society for Academic Emergency Medicine.

The two most common reasons for ordering "medically unnecessary" advanced diagnostic imaging studies were fear of missing a diagnosis despite low pretest probability, cited by 69% of respondents, and fear of litigation, cited by 64%, noted Dr. Kanzaria, a Robert Woods Johnson Foundation Clinical Scholar and emergency medicine fellow at the University of California, Los Angeles.

Patient and family expectations were identified as a driving force in ordering medically unnecessary imaging, 40% of respondents said. A mere 1% of respondents cited administrative pressure to increase group reimbursement as a main contributor, he added.

Advanced diagnostic imaging in EDs has increased appreciably in recent years, with little evidence of a resultant improvement in patient outcomes. The trend has drawn scrutiny from health policy experts in light of estimates that the U.S. annually spends $210 billion on unnecessary medical tests, procedures, and services. Yet there are little data on emergency physicians’ perceptions regarding overordering of CTs and MRIs, the causes, and the potential solutions.

"Basically, we need to know what physicians are thinking (about the issue), and that’s why we did this study," Dr. Kanzaria explained.

Two focus groups of multispecialty physicians and expert opinion from physicians who have researched overordering of diagnostic imaging were used to create the questions, which were then revised in response to a pilot study conducted among 16 emergency physicians.

The resulting 19-item survey took about 10 minutes to complete. The survey defined a "medically unnecessary" imaging study as "one you wouldn’t order if you had no external pressure and were only concerned about providing optimal medical care."

The nonrandom sample for the survey included 478 academic and community practice emergency physicians in 29 states; the completion rate was a whopping 91% (435 respondents). Respondents’ average age was 42 years with a mean 14 years in clinical practice; 68% were board-certified in emergency medicine. The pattern of survey responses did not differ based upon physician age, years in practice, or board certification status.

More than 85% of the emergency physicians said they believe too many diagnostic tests are ordered in their own ED. More specifically, a similarly lofty percentage believe medically unnecessary CTs and MRIs are ordered in their ED under common clinical scenarios described in the survey, such as head CTs for nontraumatic headaches and pan scans for trauma patients. Fully 97% of EPs acknowledged ordering medically unnecessary CTs and MRIs.

More than 50% of respondents identified as "extremely or very helpful" proposed solutions to "medically unnecessary" advanced imaging in the ED.

Topping the options was tort reform, which 79% of emergency physicians thought would make a major difference. However, Dr. Kanzaria called malpractice reform necessary but not sufficient to change practice. "Recent studies on tort reform efforts have not actually shown subsequent significant effects on cost reduction or a change in test-ordering behavior."

A more promising option may be shared decision making with patients regarding diagnostic testing for low-probability outcomes, he said. "The literature on shared decision making is still in its infancy, but what’s out there [indicates this option] is really promising as an avenue to improve communication and potentially to reduce overuse. So, I think we should consider ways to incorporate shared decision making into emergency care," Dr. Kanzaria said.

Another popular suggestion was to provide feedback to emergency physicians regarding their own test ordering behavior compared to that of their peers, something Dr. Kanzaria called "incredibly simple to do."

Education aimed at steering patients, families, and referring physicians away from the prevailing "no miss" attitude in favor of greater understanding of the probabilistic limits of diagnostic testing was also widely endorsed by the survey respondents.

Dr. Kanzaria’s research is funded by the Robert Wood Johnson Foundation Clinical Scholars Program. He reported having no financial conflicts.

[email protected]

DALLAS – On average, 22% of the CTs and MRIs ordered by emergency physicians are "medically unnecessary," based on responses by 435 emergency physicians participating in a national survey.

"The overwhelming majority of physicians in our sample recognized the issue of overimaging in the ED, and it’s not just something they felt was going on among others in their group. It’s something they personally acknowledged participating in," Dr. Hemal K. Kanzaria said at the annual meeting of the Society for Academic Emergency Medicine.

The two most common reasons for ordering "medically unnecessary" advanced diagnostic imaging studies were fear of missing a diagnosis despite low pretest probability, cited by 69% of respondents, and fear of litigation, cited by 64%, noted Dr. Kanzaria, a Robert Woods Johnson Foundation Clinical Scholar and emergency medicine fellow at the University of California, Los Angeles.

Patient and family expectations were identified as a driving force in ordering medically unnecessary imaging, 40% of respondents said. A mere 1% of respondents cited administrative pressure to increase group reimbursement as a main contributor, he added.

Advanced diagnostic imaging in EDs has increased appreciably in recent years, with little evidence of a resultant improvement in patient outcomes. The trend has drawn scrutiny from health policy experts in light of estimates that the U.S. annually spends $210 billion on unnecessary medical tests, procedures, and services. Yet there are little data on emergency physicians’ perceptions regarding overordering of CTs and MRIs, the causes, and the potential solutions.

"Basically, we need to know what physicians are thinking (about the issue), and that’s why we did this study," Dr. Kanzaria explained.

Two focus groups of multispecialty physicians and expert opinion from physicians who have researched overordering of diagnostic imaging were used to create the questions, which were then revised in response to a pilot study conducted among 16 emergency physicians.

The resulting 19-item survey took about 10 minutes to complete. The survey defined a "medically unnecessary" imaging study as "one you wouldn’t order if you had no external pressure and were only concerned about providing optimal medical care."

The nonrandom sample for the survey included 478 academic and community practice emergency physicians in 29 states; the completion rate was a whopping 91% (435 respondents). Respondents’ average age was 42 years with a mean 14 years in clinical practice; 68% were board-certified in emergency medicine. The pattern of survey responses did not differ based upon physician age, years in practice, or board certification status.

More than 85% of the emergency physicians said they believe too many diagnostic tests are ordered in their own ED. More specifically, a similarly lofty percentage believe medically unnecessary CTs and MRIs are ordered in their ED under common clinical scenarios described in the survey, such as head CTs for nontraumatic headaches and pan scans for trauma patients. Fully 97% of EPs acknowledged ordering medically unnecessary CTs and MRIs.

More than 50% of respondents identified as "extremely or very helpful" proposed solutions to "medically unnecessary" advanced imaging in the ED.

Topping the options was tort reform, which 79% of emergency physicians thought would make a major difference. However, Dr. Kanzaria called malpractice reform necessary but not sufficient to change practice. "Recent studies on tort reform efforts have not actually shown subsequent significant effects on cost reduction or a change in test-ordering behavior."

A more promising option may be shared decision making with patients regarding diagnostic testing for low-probability outcomes, he said. "The literature on shared decision making is still in its infancy, but what’s out there [indicates this option] is really promising as an avenue to improve communication and potentially to reduce overuse. So, I think we should consider ways to incorporate shared decision making into emergency care," Dr. Kanzaria said.

Another popular suggestion was to provide feedback to emergency physicians regarding their own test ordering behavior compared to that of their peers, something Dr. Kanzaria called "incredibly simple to do."

Education aimed at steering patients, families, and referring physicians away from the prevailing "no miss" attitude in favor of greater understanding of the probabilistic limits of diagnostic testing was also widely endorsed by the survey respondents.

Dr. Kanzaria’s research is funded by the Robert Wood Johnson Foundation Clinical Scholars Program. He reported having no financial conflicts.

[email protected]

DALLAS – On average, 22% of the CTs and MRIs ordered by emergency physicians are "medically unnecessary," based on responses by 435 emergency physicians participating in a national survey.

"The overwhelming majority of physicians in our sample recognized the issue of overimaging in the ED, and it’s not just something they felt was going on among others in their group. It’s something they personally acknowledged participating in," Dr. Hemal K. Kanzaria said at the annual meeting of the Society for Academic Emergency Medicine.

The two most common reasons for ordering "medically unnecessary" advanced diagnostic imaging studies were fear of missing a diagnosis despite low pretest probability, cited by 69% of respondents, and fear of litigation, cited by 64%, noted Dr. Kanzaria, a Robert Woods Johnson Foundation Clinical Scholar and emergency medicine fellow at the University of California, Los Angeles.

Patient and family expectations were identified as a driving force in ordering medically unnecessary imaging, 40% of respondents said. A mere 1% of respondents cited administrative pressure to increase group reimbursement as a main contributor, he added.

Advanced diagnostic imaging in EDs has increased appreciably in recent years, with little evidence of a resultant improvement in patient outcomes. The trend has drawn scrutiny from health policy experts in light of estimates that the U.S. annually spends $210 billion on unnecessary medical tests, procedures, and services. Yet there are little data on emergency physicians’ perceptions regarding overordering of CTs and MRIs, the causes, and the potential solutions.

"Basically, we need to know what physicians are thinking (about the issue), and that’s why we did this study," Dr. Kanzaria explained.

Two focus groups of multispecialty physicians and expert opinion from physicians who have researched overordering of diagnostic imaging were used to create the questions, which were then revised in response to a pilot study conducted among 16 emergency physicians.

The resulting 19-item survey took about 10 minutes to complete. The survey defined a "medically unnecessary" imaging study as "one you wouldn’t order if you had no external pressure and were only concerned about providing optimal medical care."

The nonrandom sample for the survey included 478 academic and community practice emergency physicians in 29 states; the completion rate was a whopping 91% (435 respondents). Respondents’ average age was 42 years with a mean 14 years in clinical practice; 68% were board-certified in emergency medicine. The pattern of survey responses did not differ based upon physician age, years in practice, or board certification status.

More than 85% of the emergency physicians said they believe too many diagnostic tests are ordered in their own ED. More specifically, a similarly lofty percentage believe medically unnecessary CTs and MRIs are ordered in their ED under common clinical scenarios described in the survey, such as head CTs for nontraumatic headaches and pan scans for trauma patients. Fully 97% of EPs acknowledged ordering medically unnecessary CTs and MRIs.

More than 50% of respondents identified as "extremely or very helpful" proposed solutions to "medically unnecessary" advanced imaging in the ED.

Topping the options was tort reform, which 79% of emergency physicians thought would make a major difference. However, Dr. Kanzaria called malpractice reform necessary but not sufficient to change practice. "Recent studies on tort reform efforts have not actually shown subsequent significant effects on cost reduction or a change in test-ordering behavior."

A more promising option may be shared decision making with patients regarding diagnostic testing for low-probability outcomes, he said. "The literature on shared decision making is still in its infancy, but what’s out there [indicates this option] is really promising as an avenue to improve communication and potentially to reduce overuse. So, I think we should consider ways to incorporate shared decision making into emergency care," Dr. Kanzaria said.

Another popular suggestion was to provide feedback to emergency physicians regarding their own test ordering behavior compared to that of their peers, something Dr. Kanzaria called "incredibly simple to do."

Education aimed at steering patients, families, and referring physicians away from the prevailing "no miss" attitude in favor of greater understanding of the probabilistic limits of diagnostic testing was also widely endorsed by the survey respondents.

Dr. Kanzaria’s research is funded by the Robert Wood Johnson Foundation Clinical Scholars Program. He reported having no financial conflicts.

[email protected]

PHILADELPHIA – Patients who have migraines and comorbid psychiatric disorders visited the emergency department more, and received more brain imaging and narcotics, than patients who had only migraine.

The additional emergency visits and procedures – combined with significantly higher rates of hospital admissions and outpatient visits – run contrary to published recommendations, Dr. Mia Minen reported at the annual meeting of the American Academy of Neurology.

The imaging findings of her cross-sectional analysis are particularly troubling in light of current guidelines aimed at helping to minimize radiation exposure by avoiding head and brain imaging in patients with primary headache disorders, said Dr. Minen, a fellow at the Graham Headache Center, Boston.

"One of the AAN’s recommendations for the Choosing Wisely campaign was not to perform brain imaging for patients presenting to the ED with recurrence of their baseline primary headache disorder," she said. She added that the American College of Emergency Physicians has not found level A evidence supporting imaging in patients who present to the emergency department with headache, unless the headache is sudden and severe, or unless it’s accompanied by an abnormal neurological exam.

Her analysis looked at emergency treatment trends in a database of almost 3,000 headache patients seen over a 10-year period in a single hospital’s emergency department. The patients were a mean of 40 years old; most (80%) were women. About 2,000 had at least one psychiatric comorbidity; the most common psychiatric comorbidities were anxiety and depression.

Over the 10-year study period, migraine patients overall made an average of 11 ED visits, with 10 admissions and 26 outpatient visits. Those patients without a comorbid psychiatric diagnosis made significantly fewer visits in every category: 6 ED visits, 3 inpatient visits, and 11 outpatient visits.

Migraine patients with comorbidities presented a very different picture, Dr. Minen said. These patients had an average of 18 ED visits, 19 inpatient visits, and 45 outpatient visits over the study period.

Compared with migraineurs without psychiatric disorders, those with them were significantly more likely to undergo a CT of the head (relative risk, 1.4) and an MRI of the brain (RR, 1.5). They received narcotic treatment in the ED significantly more often as well.

"We need more studies to understand why this is the case," Dr. Minen said.

She added that the pharmacotherapy findings also were in contrast to recommendations in the AAN Choosing Wisely campaign.

"In 2013, one of the final recommendations was not to use opiates or butalbital for the treatment of migraine, except in rare circumstances."

Dr. Minen had no financial disclosures.

[email protected]

PHILADELPHIA – Patients who have migraines and comorbid psychiatric disorders visited the emergency department more, and received more brain imaging and narcotics, than patients who had only migraine.

The additional emergency visits and procedures – combined with significantly higher rates of hospital admissions and outpatient visits – run contrary to published recommendations, Dr. Mia Minen reported at the annual meeting of the American Academy of Neurology.

The imaging findings of her cross-sectional analysis are particularly troubling in light of current guidelines aimed at helping to minimize radiation exposure by avoiding head and brain imaging in patients with primary headache disorders, said Dr. Minen, a fellow at the Graham Headache Center, Boston.

"One of the AAN’s recommendations for the Choosing Wisely campaign was not to perform brain imaging for patients presenting to the ED with recurrence of their baseline primary headache disorder," she said. She added that the American College of Emergency Physicians has not found level A evidence supporting imaging in patients who present to the emergency department with headache, unless the headache is sudden and severe, or unless it’s accompanied by an abnormal neurological exam.

Her analysis looked at emergency treatment trends in a database of almost 3,000 headache patients seen over a 10-year period in a single hospital’s emergency department. The patients were a mean of 40 years old; most (80%) were women. About 2,000 had at least one psychiatric comorbidity; the most common psychiatric comorbidities were anxiety and depression.

Over the 10-year study period, migraine patients overall made an average of 11 ED visits, with 10 admissions and 26 outpatient visits. Those patients without a comorbid psychiatric diagnosis made significantly fewer visits in every category: 6 ED visits, 3 inpatient visits, and 11 outpatient visits.

Migraine patients with comorbidities presented a very different picture, Dr. Minen said. These patients had an average of 18 ED visits, 19 inpatient visits, and 45 outpatient visits over the study period.

Compared with migraineurs without psychiatric disorders, those with them were significantly more likely to undergo a CT of the head (relative risk, 1.4) and an MRI of the brain (RR, 1.5). They received narcotic treatment in the ED significantly more often as well.

"We need more studies to understand why this is the case," Dr. Minen said.

She added that the pharmacotherapy findings also were in contrast to recommendations in the AAN Choosing Wisely campaign.

"In 2013, one of the final recommendations was not to use opiates or butalbital for the treatment of migraine, except in rare circumstances."

Dr. Minen had no financial disclosures.

[email protected]

PHILADELPHIA – Patients who have migraines and comorbid psychiatric disorders visited the emergency department more, and received more brain imaging and narcotics, than patients who had only migraine.

The additional emergency visits and procedures – combined with significantly higher rates of hospital admissions and outpatient visits – run contrary to published recommendations, Dr. Mia Minen reported at the annual meeting of the American Academy of Neurology.

The imaging findings of her cross-sectional analysis are particularly troubling in light of current guidelines aimed at helping to minimize radiation exposure by avoiding head and brain imaging in patients with primary headache disorders, said Dr. Minen, a fellow at the Graham Headache Center, Boston.

"One of the AAN’s recommendations for the Choosing Wisely campaign was not to perform brain imaging for patients presenting to the ED with recurrence of their baseline primary headache disorder," she said. She added that the American College of Emergency Physicians has not found level A evidence supporting imaging in patients who present to the emergency department with headache, unless the headache is sudden and severe, or unless it’s accompanied by an abnormal neurological exam.

Her analysis looked at emergency treatment trends in a database of almost 3,000 headache patients seen over a 10-year period in a single hospital’s emergency department. The patients were a mean of 40 years old; most (80%) were women. About 2,000 had at least one psychiatric comorbidity; the most common psychiatric comorbidities were anxiety and depression.

Over the 10-year study period, migraine patients overall made an average of 11 ED visits, with 10 admissions and 26 outpatient visits. Those patients without a comorbid psychiatric diagnosis made significantly fewer visits in every category: 6 ED visits, 3 inpatient visits, and 11 outpatient visits.

Migraine patients with comorbidities presented a very different picture, Dr. Minen said. These patients had an average of 18 ED visits, 19 inpatient visits, and 45 outpatient visits over the study period.

Compared with migraineurs without psychiatric disorders, those with them were significantly more likely to undergo a CT of the head (relative risk, 1.4) and an MRI of the brain (RR, 1.5). They received narcotic treatment in the ED significantly more often as well.

"We need more studies to understand why this is the case," Dr. Minen said.

She added that the pharmacotherapy findings also were in contrast to recommendations in the AAN Choosing Wisely campaign.

"In 2013, one of the final recommendations was not to use opiates or butalbital for the treatment of migraine, except in rare circumstances."

Dr. Minen had no financial disclosures.

[email protected]

Children with heart disease are cumulatively exposed to relatively low levels of ionizing radiation from imaging procedures – less than the average annual background exposure in the United States – although those who have undergone more complex procedures such as heart transplants or cardiac catheterization experience significantly greater exposure, a retrospective cohort study has found.

Dr. Jason N. Johnson, a pediatric cardiologist at Duke University Medical Center, Durham, N.C., and his colleagues showed that the estimated lifetime attributable risk of cancer above baseline ranged from 6 cases per 100,000 exposed for children with atrial septal defect, to 1,677 per 100,000 exposed for cardiac transplant, with a median of 65 cases per 100,000 across surgical cohorts.

While conventional radiographic examination accounted for 92% of the total examinations, it accounted for only 8% of the cumulative effective dose, compared with cardiac catheterization, which represented 1.5% of all examinations but accounted for 60% of the total radiation exposure, according to a study published online June 9 in Circulation.

The study of 337 children aged 6 years or younger exposed to more than 13,000 radiation examinations found the lifetime attributable risk of cancer was nearly double in females versus males, mostly because of increased breast and thyroid cancer risk (Circulation 2014 June 9 [doi:10.1161/CIRCULATIONAHA.113.005425]).

The study was funded by grants from the National Institutes of Health and the Mend a Heart Foundation. One author reported receiving support from the U.S. Nuclear Regulatory Commission, the U.S. Department of Energy, and Duke University.

Children with heart disease are cumulatively exposed to relatively low levels of ionizing radiation from imaging procedures – less than the average annual background exposure in the United States – although those who have undergone more complex procedures such as heart transplants or cardiac catheterization experience significantly greater exposure, a retrospective cohort study has found.

Dr. Jason N. Johnson, a pediatric cardiologist at Duke University Medical Center, Durham, N.C., and his colleagues showed that the estimated lifetime attributable risk of cancer above baseline ranged from 6 cases per 100,000 exposed for children with atrial septal defect, to 1,677 per 100,000 exposed for cardiac transplant, with a median of 65 cases per 100,000 across surgical cohorts.

While conventional radiographic examination accounted for 92% of the total examinations, it accounted for only 8% of the cumulative effective dose, compared with cardiac catheterization, which represented 1.5% of all examinations but accounted for 60% of the total radiation exposure, according to a study published online June 9 in Circulation.

The study of 337 children aged 6 years or younger exposed to more than 13,000 radiation examinations found the lifetime attributable risk of cancer was nearly double in females versus males, mostly because of increased breast and thyroid cancer risk (Circulation 2014 June 9 [doi:10.1161/CIRCULATIONAHA.113.005425]).

The study was funded by grants from the National Institutes of Health and the Mend a Heart Foundation. One author reported receiving support from the U.S. Nuclear Regulatory Commission, the U.S. Department of Energy, and Duke University.

Children with heart disease are cumulatively exposed to relatively low levels of ionizing radiation from imaging procedures – less than the average annual background exposure in the United States – although those who have undergone more complex procedures such as heart transplants or cardiac catheterization experience significantly greater exposure, a retrospective cohort study has found.

Dr. Jason N. Johnson, a pediatric cardiologist at Duke University Medical Center, Durham, N.C., and his colleagues showed that the estimated lifetime attributable risk of cancer above baseline ranged from 6 cases per 100,000 exposed for children with atrial septal defect, to 1,677 per 100,000 exposed for cardiac transplant, with a median of 65 cases per 100,000 across surgical cohorts.

While conventional radiographic examination accounted for 92% of the total examinations, it accounted for only 8% of the cumulative effective dose, compared with cardiac catheterization, which represented 1.5% of all examinations but accounted for 60% of the total radiation exposure, according to a study published online June 9 in Circulation.

The study of 337 children aged 6 years or younger exposed to more than 13,000 radiation examinations found the lifetime attributable risk of cancer was nearly double in females versus males, mostly because of increased breast and thyroid cancer risk (Circulation 2014 June 9 [doi:10.1161/CIRCULATIONAHA.113.005425]).

The study was funded by grants from the National Institutes of Health and the Mend a Heart Foundation. One author reported receiving support from the U.S. Nuclear Regulatory Commission, the U.S. Department of Energy, and Duke University.

When it comes to diagnostic imaging, the average costs of angiograms, abdominal CTs, and MRIs are higher in the United States than in other industrialized countries, according to the International Federation of Health Plans’ 2013 Comparative Price Report.

The average cost of an angiogram in the United States last year was $907, about 11% higher than Argentina’s $818, which was the second-highest of the six countries included in all three IFHP comparisons. The lowest cost among the six countries was in the Netherlands, at $174.

For an abdominal CT scan, the average cost in the United States was $896 in 2013, compared with $500 in Australia. Spain had the lowest cost, with an average of $94, the IFHP reported. In the United States, the average price for an MRI in 2013 was $1,145, with the Netherlands second at $461 and Switzerland lowest at $138.

New Zealand, which was not included in the angiogram analysis and therefore left out of the graph below, was actually the second most-expensive country in which to get a CT scan ($731) and an MRI ($1,005).

The IFHP is composed of more than 100 member companies in 25 countries. For the survey, the price for each country was submitted by participating member plans. Some prices are drawn from the public sector, and some are from the private sector. U.S. averages are calculated from more than 100 million claims in the Truven MarketScan Research databases.

[email protected]

When it comes to diagnostic imaging, the average costs of angiograms, abdominal CTs, and MRIs are higher in the United States than in other industrialized countries, according to the International Federation of Health Plans’ 2013 Comparative Price Report.

The average cost of an angiogram in the United States last year was $907, about 11% higher than Argentina’s $818, which was the second-highest of the six countries included in all three IFHP comparisons. The lowest cost among the six countries was in the Netherlands, at $174.

For an abdominal CT scan, the average cost in the United States was $896 in 2013, compared with $500 in Australia. Spain had the lowest cost, with an average of $94, the IFHP reported. In the United States, the average price for an MRI in 2013 was $1,145, with the Netherlands second at $461 and Switzerland lowest at $138.

New Zealand, which was not included in the angiogram analysis and therefore left out of the graph below, was actually the second most-expensive country in which to get a CT scan ($731) and an MRI ($1,005).

The IFHP is composed of more than 100 member companies in 25 countries. For the survey, the price for each country was submitted by participating member plans. Some prices are drawn from the public sector, and some are from the private sector. U.S. averages are calculated from more than 100 million claims in the Truven MarketScan Research databases.

[email protected]

When it comes to diagnostic imaging, the average costs of angiograms, abdominal CTs, and MRIs are higher in the United States than in other industrialized countries, according to the International Federation of Health Plans’ 2013 Comparative Price Report.

The average cost of an angiogram in the United States last year was $907, about 11% higher than Argentina’s $818, which was the second-highest of the six countries included in all three IFHP comparisons. The lowest cost among the six countries was in the Netherlands, at $174.

For an abdominal CT scan, the average cost in the United States was $896 in 2013, compared with $500 in Australia. Spain had the lowest cost, with an average of $94, the IFHP reported. In the United States, the average price for an MRI in 2013 was $1,145, with the Netherlands second at $461 and Switzerland lowest at $138.

New Zealand, which was not included in the angiogram analysis and therefore left out of the graph below, was actually the second most-expensive country in which to get a CT scan ($731) and an MRI ($1,005).

The IFHP is composed of more than 100 member companies in 25 countries. For the survey, the price for each country was submitted by participating member plans. Some prices are drawn from the public sector, and some are from the private sector. U.S. averages are calculated from more than 100 million claims in the Truven MarketScan Research databases.

[email protected]

Case

A 3-year-old girl presented to the ED with a 1-week history of cough and new-onset abdominal pain. She was accompanied by her grandfather, who stated that the child had been dropped-off at his house around 5:00 pm the previous day. He noted that after putting his granddaughter to bed, she awoke around 4:30 am complaining of a stomachache. After rocking her, he said she went back to sleep but did not wake up again until 1:00 pm that afternoon. Over the first few hours of awakening, she became less active and had three episodes of posttussive emesis. The grandfather denied the child had any recent nasal congestion, fever, nausea, vomiting, or diarrhea. When questioned about possible toxic ingestion, he said there were no medications in the house and that he did not witness any substance ingestion or trauma.

Regarding history, the patient was born full-term without any complications. She did not have any significant medical or surgical history. There were no documented allergies, and she was not on any medications. All of her immunizations were up-to-date. The family history was not significant for chronic diseases except for asthma in distant relatives. Her grandfather denied any recent exposures or travel.

At presentation, the patient’s vital signs were: blood pressure (BP) 86/49 mm Hg; heart rate (HR), 178 beats/minute and regular; respiratory rate (RR), 26 breaths/minute; temporal artery temperature, 104.7°F. Oxygen saturation was 99% on room air. On physical examination, she was normocephalic; there was no scleral icterus; and the throat and bilateral tympanic membranes were normal. Her extremities were warm and well perfused, with normal capillary refill. Patient’s lungs were clear, and heart sounds were normal with no detection of a murmur. The abdomen was soft and nontender; there was no evidence of organomegaly.

Laboratory evaluation included assessment of sodium, chloride, carbon dioxide, calcium, magnesium, amylase, lipase, and creatine levels; liver function test; complete blood count; and red-cell indices. All of the laboratory values were within normal limits, and urinalysis was negative for infection. Blood and urine cultures were also taken. A chest X-ray showed no acute intrathoracic process (Figure 1).

Secondary to the patient’s fever and tachycardia, the presumed diagnosis was systemic inflammatory response syndrome, and an intravenous (IV) bolus of normal saline 20 mL/kg along with ibuprofen and ondansetron were administered to treat fever and nausea, respectively. In addition, a dose of ceftriaxone was also given. The patient’s repeat set of vitals were: BP, 86/64 mm Hg; HR, 195 beats/minute; RR, 20 breaths/minute; and temporal artery temperature, 97.9°F; oxygen saturation was 98% on room air.

During treatment, the patient became increasingly fussy with new-onset abdominal distension. Repeat physical examination revealed hepatomegaly. A bedside echocardiogram showed hyperdynamic heart with fractional shortening* (FS) of 20% and ejection fraction (EF) of 43%, but no structural abnormalities. An electrocardiogram (ECG) was then ordered, which revealed narrow complex tachycardia with inverted P-waves in inferior leads.

The patient was transferred to the intensive care unit where she was started on IV milrinone for development of secondary hypotension and reduced cardiac function. Based on inverted P waves on ECG leads II, III, and aVF, three doses of adenosine (0.1 mg/kg, 0.2 mg/kg, and 0.2 mg/kg) were given, which interrupted the tachycafrdia for only a few beats. After consultation with a cardiac electrophysiologist, a diagnosis of persistent junctional reentrant tachycardia (PJRT) was reached based on the patient’s ECG features and nonresponse to adenosine. She was started on IV amiodarone (loading dose of 5 mg/kg followed by infusion of 5 mcg/kg/min), which relieved the tachycardia (Figure 3). Her vital signs stabilized and her clinical status gradually improved. After 3 days, she was discharged on oral amiodarone and close follow-up with cardiology. A repeat echocardiogram just prior to discharge showed improvement in FS to 23% and EF to 48%.

Discussion

Normal cardiac conduction involves an originating impulse from a sinus node followed by atrial muscle activation reaching the atrioventricular (AV) node. There is a necessary delay at the AV node, which is required for ventricular filling and activation of ventricles through the His-Purkinje fiber system and the bundle branches. An abnormality or interruption of this pathway results in an arrhythmia such as supraventricular tachycardia (SVT).

Supraventricular Tachycardia

Supraventricular tachycardia is the most common symptomatic abnormality in the pediatric population.¹ Among the various forms of SVT, AV reentrant tachycardia (AVRT) and AV node reentrant tachycardia (AVNRT) account for most case presentations.² Supraventricular tachycardia may be classified by duration of RP interval compared to PR interval on ECG. Short RP interval SVT includes AVNRT and AVRT through a rapidly conducting accessory path. Long RP interval SVT includes atypical AVNRT, atrial tachycardia, and PJRT.

 

Persistent Junctional Reentrant Tachycardia

Persistent junctional reentrant tachycardia is a rare form of long RP tachycardia, accounting for approximately 1% of SVT in a study review of 21 patients.³ As with the patient in this case, PJRT usually presents in early childhood.³   In a recent review of 194 patients with PJRT, 57% were infants.⁴ The condition involves an accessory pathway most commonly located in the posterior-superior septal region; conduction involves a retrograde impulse through the decremental accessory pathway.⁵ On ECG, findings include a negative P wave in inferior leads, a long RP interval, and a 1:1 AV conduction.⁶

A long-term multicenter follow-up study of 32 patients showed that rates of tachycardia vary among patients, from 100 to 250 beats/minute.⁷ Tachycardia-induced cardiomyopathy (TIC), which is secondary to the incessant nature of tachycardia, may be present in up to 30% to 50% of patients.^3,8 In a recent multicenter study, PJRT was responsible for 23% of cases of TIC.⁹ Although the exact mechanism of this property is unknown, decremental conduction and unidirectional block of the accessory pathway appear to be contributing factors.⁶

Treatment

Adenosine is the initial drug of choice for narrow complex tachycardia with stable hemodynamic status and an available intravascular access.¹⁰ In a study evaluating the effectiveness of adenosine for managing SVT in the pediatric ED setting, it was more than 70% effective in cardioverting patients presumed to have SVT.¹¹ However, in PJRT, owing to the incessant pattern, adenosine may either terminate the tachycardia (causing asystole) or, as seen in this patient, convert tachycardia to sinus rhythm for only a few seconds.¹² Reinitiation of tachycardia in sinus beat without the need for a premature complex contributes to its incessant nature.¹³

In a multicenter study looking at clinical profile and outcome for PJRT, Vaksmann et al⁸ found a greater than 80% success rate in controlling the dysrhythmia with amiodarone and verapamil. For long-term management of tachyarrhythmia, medical therapy has been recommended in early childhood compared to older children in whom catheter ablation is an effective approach.⁷ Spontaneous resolution of PJRT has been documented but is rare.¹⁴

Conclusion

Pediatric cardiac emergencies require very specific treatment. As such, it is important that the emergency physician distinguish the different the types of tachyarrhythmias—especially in cases that do not respond to treatment with adenosine. In the pediatric patient, PJRT is a potentially life-threatening arrhythmia that requires a high index of suspicion. Clues to diagnosis include negative P waves in inferior leads, long RP interval, and 1:1 atrioventricular conduction.

Dr Fichadia is a fellow, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan. Dr Perez is a clinical instructor, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan.

Case

A 3-year-old girl presented to the ED with a 1-week history of cough and new-onset abdominal pain. She was accompanied by her grandfather, who stated that the child had been dropped-off at his house around 5:00 pm the previous day. He noted that after putting his granddaughter to bed, she awoke around 4:30 am complaining of a stomachache. After rocking her, he said she went back to sleep but did not wake up again until 1:00 pm that afternoon. Over the first few hours of awakening, she became less active and had three episodes of posttussive emesis. The grandfather denied the child had any recent nasal congestion, fever, nausea, vomiting, or diarrhea. When questioned about possible toxic ingestion, he said there were no medications in the house and that he did not witness any substance ingestion or trauma.

Regarding history, the patient was born full-term without any complications. She did not have any significant medical or surgical history. There were no documented allergies, and she was not on any medications. All of her immunizations were up-to-date. The family history was not significant for chronic diseases except for asthma in distant relatives. Her grandfather denied any recent exposures or travel.

At presentation, the patient’s vital signs were: blood pressure (BP) 86/49 mm Hg; heart rate (HR), 178 beats/minute and regular; respiratory rate (RR), 26 breaths/minute; temporal artery temperature, 104.7°F. Oxygen saturation was 99% on room air. On physical examination, she was normocephalic; there was no scleral icterus; and the throat and bilateral tympanic membranes were normal. Her extremities were warm and well perfused, with normal capillary refill. Patient’s lungs were clear, and heart sounds were normal with no detection of a murmur. The abdomen was soft and nontender; there was no evidence of organomegaly.

Laboratory evaluation included assessment of sodium, chloride, carbon dioxide, calcium, magnesium, amylase, lipase, and creatine levels; liver function test; complete blood count; and red-cell indices. All of the laboratory values were within normal limits, and urinalysis was negative for infection. Blood and urine cultures were also taken. A chest X-ray showed no acute intrathoracic process (Figure 1).

Secondary to the patient’s fever and tachycardia, the presumed diagnosis was systemic inflammatory response syndrome, and an intravenous (IV) bolus of normal saline 20 mL/kg along with ibuprofen and ondansetron were administered to treat fever and nausea, respectively. In addition, a dose of ceftriaxone was also given. The patient’s repeat set of vitals were: BP, 86/64 mm Hg; HR, 195 beats/minute; RR, 20 breaths/minute; and temporal artery temperature, 97.9°F; oxygen saturation was 98% on room air.

During treatment, the patient became increasingly fussy with new-onset abdominal distension. Repeat physical examination revealed hepatomegaly. A bedside echocardiogram showed hyperdynamic heart with fractional shortening* (FS) of 20% and ejection fraction (EF) of 43%, but no structural abnormalities. An electrocardiogram (ECG) was then ordered, which revealed narrow complex tachycardia with inverted P-waves in inferior leads.

The patient was transferred to the intensive care unit where she was started on IV milrinone for development of secondary hypotension and reduced cardiac function. Based on inverted P waves on ECG leads II, III, and aVF, three doses of adenosine (0.1 mg/kg, 0.2 mg/kg, and 0.2 mg/kg) were given, which interrupted the tachycafrdia for only a few beats. After consultation with a cardiac electrophysiologist, a diagnosis of persistent junctional reentrant tachycardia (PJRT) was reached based on the patient’s ECG features and nonresponse to adenosine. She was started on IV amiodarone (loading dose of 5 mg/kg followed by infusion of 5 mcg/kg/min), which relieved the tachycardia (Figure 3). Her vital signs stabilized and her clinical status gradually improved. After 3 days, she was discharged on oral amiodarone and close follow-up with cardiology. A repeat echocardiogram just prior to discharge showed improvement in FS to 23% and EF to 48%.

Discussion

Normal cardiac conduction involves an originating impulse from a sinus node followed by atrial muscle activation reaching the atrioventricular (AV) node. There is a necessary delay at the AV node, which is required for ventricular filling and activation of ventricles through the His-Purkinje fiber system and the bundle branches. An abnormality or interruption of this pathway results in an arrhythmia such as supraventricular tachycardia (SVT).

Supraventricular Tachycardia

Supraventricular tachycardia is the most common symptomatic abnormality in the pediatric population.¹ Among the various forms of SVT, AV reentrant tachycardia (AVRT) and AV node reentrant tachycardia (AVNRT) account for most case presentations.² Supraventricular tachycardia may be classified by duration of RP interval compared to PR interval on ECG. Short RP interval SVT includes AVNRT and AVRT through a rapidly conducting accessory path. Long RP interval SVT includes atypical AVNRT, atrial tachycardia, and PJRT.

 

Persistent Junctional Reentrant Tachycardia

Persistent junctional reentrant tachycardia is a rare form of long RP tachycardia, accounting for approximately 1% of SVT in a study review of 21 patients.³ As with the patient in this case, PJRT usually presents in early childhood.³   In a recent review of 194 patients with PJRT, 57% were infants.⁴ The condition involves an accessory pathway most commonly located in the posterior-superior septal region; conduction involves a retrograde impulse through the decremental accessory pathway.⁵ On ECG, findings include a negative P wave in inferior leads, a long RP interval, and a 1:1 AV conduction.⁶

A long-term multicenter follow-up study of 32 patients showed that rates of tachycardia vary among patients, from 100 to 250 beats/minute.⁷ Tachycardia-induced cardiomyopathy (TIC), which is secondary to the incessant nature of tachycardia, may be present in up to 30% to 50% of patients.^3,8 In a recent multicenter study, PJRT was responsible for 23% of cases of TIC.⁹ Although the exact mechanism of this property is unknown, decremental conduction and unidirectional block of the accessory pathway appear to be contributing factors.⁶

Treatment

Adenosine is the initial drug of choice for narrow complex tachycardia with stable hemodynamic status and an available intravascular access.¹⁰ In a study evaluating the effectiveness of adenosine for managing SVT in the pediatric ED setting, it was more than 70% effective in cardioverting patients presumed to have SVT.¹¹ However, in PJRT, owing to the incessant pattern, adenosine may either terminate the tachycardia (causing asystole) or, as seen in this patient, convert tachycardia to sinus rhythm for only a few seconds.¹² Reinitiation of tachycardia in sinus beat without the need for a premature complex contributes to its incessant nature.¹³

In a multicenter study looking at clinical profile and outcome for PJRT, Vaksmann et al⁸ found a greater than 80% success rate in controlling the dysrhythmia with amiodarone and verapamil. For long-term management of tachyarrhythmia, medical therapy has been recommended in early childhood compared to older children in whom catheter ablation is an effective approach.⁷ Spontaneous resolution of PJRT has been documented but is rare.¹⁴

Conclusion

Pediatric cardiac emergencies require very specific treatment. As such, it is important that the emergency physician distinguish the different the types of tachyarrhythmias—especially in cases that do not respond to treatment with adenosine. In the pediatric patient, PJRT is a potentially life-threatening arrhythmia that requires a high index of suspicion. Clues to diagnosis include negative P waves in inferior leads, long RP interval, and 1:1 atrioventricular conduction.

Dr Fichadia is a fellow, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan. Dr Perez is a clinical instructor, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan.

Case

A 3-year-old girl presented to the ED with a 1-week history of cough and new-onset abdominal pain. She was accompanied by her grandfather, who stated that the child had been dropped-off at his house around 5:00 pm the previous day. He noted that after putting his granddaughter to bed, she awoke around 4:30 am complaining of a stomachache. After rocking her, he said she went back to sleep but did not wake up again until 1:00 pm that afternoon. Over the first few hours of awakening, she became less active and had three episodes of posttussive emesis. The grandfather denied the child had any recent nasal congestion, fever, nausea, vomiting, or diarrhea. When questioned about possible toxic ingestion, he said there were no medications in the house and that he did not witness any substance ingestion or trauma.

Regarding history, the patient was born full-term without any complications. She did not have any significant medical or surgical history. There were no documented allergies, and she was not on any medications. All of her immunizations were up-to-date. The family history was not significant for chronic diseases except for asthma in distant relatives. Her grandfather denied any recent exposures or travel.

At presentation, the patient’s vital signs were: blood pressure (BP) 86/49 mm Hg; heart rate (HR), 178 beats/minute and regular; respiratory rate (RR), 26 breaths/minute; temporal artery temperature, 104.7°F. Oxygen saturation was 99% on room air. On physical examination, she was normocephalic; there was no scleral icterus; and the throat and bilateral tympanic membranes were normal. Her extremities were warm and well perfused, with normal capillary refill. Patient’s lungs were clear, and heart sounds were normal with no detection of a murmur. The abdomen was soft and nontender; there was no evidence of organomegaly.

Laboratory evaluation included assessment of sodium, chloride, carbon dioxide, calcium, magnesium, amylase, lipase, and creatine levels; liver function test; complete blood count; and red-cell indices. All of the laboratory values were within normal limits, and urinalysis was negative for infection. Blood and urine cultures were also taken. A chest X-ray showed no acute intrathoracic process (Figure 1).

Secondary to the patient’s fever and tachycardia, the presumed diagnosis was systemic inflammatory response syndrome, and an intravenous (IV) bolus of normal saline 20 mL/kg along with ibuprofen and ondansetron were administered to treat fever and nausea, respectively. In addition, a dose of ceftriaxone was also given. The patient’s repeat set of vitals were: BP, 86/64 mm Hg; HR, 195 beats/minute; RR, 20 breaths/minute; and temporal artery temperature, 97.9°F; oxygen saturation was 98% on room air.

During treatment, the patient became increasingly fussy with new-onset abdominal distension. Repeat physical examination revealed hepatomegaly. A bedside echocardiogram showed hyperdynamic heart with fractional shortening* (FS) of 20% and ejection fraction (EF) of 43%, but no structural abnormalities. An electrocardiogram (ECG) was then ordered, which revealed narrow complex tachycardia with inverted P-waves in inferior leads.

The patient was transferred to the intensive care unit where she was started on IV milrinone for development of secondary hypotension and reduced cardiac function. Based on inverted P waves on ECG leads II, III, and aVF, three doses of adenosine (0.1 mg/kg, 0.2 mg/kg, and 0.2 mg/kg) were given, which interrupted the tachycafrdia for only a few beats. After consultation with a cardiac electrophysiologist, a diagnosis of persistent junctional reentrant tachycardia (PJRT) was reached based on the patient’s ECG features and nonresponse to adenosine. She was started on IV amiodarone (loading dose of 5 mg/kg followed by infusion of 5 mcg/kg/min), which relieved the tachycardia (Figure 3). Her vital signs stabilized and her clinical status gradually improved. After 3 days, she was discharged on oral amiodarone and close follow-up with cardiology. A repeat echocardiogram just prior to discharge showed improvement in FS to 23% and EF to 48%.

Discussion

Normal cardiac conduction involves an originating impulse from a sinus node followed by atrial muscle activation reaching the atrioventricular (AV) node. There is a necessary delay at the AV node, which is required for ventricular filling and activation of ventricles through the His-Purkinje fiber system and the bundle branches. An abnormality or interruption of this pathway results in an arrhythmia such as supraventricular tachycardia (SVT).

Supraventricular Tachycardia

Supraventricular tachycardia is the most common symptomatic abnormality in the pediatric population.¹ Among the various forms of SVT, AV reentrant tachycardia (AVRT) and AV node reentrant tachycardia (AVNRT) account for most case presentations.² Supraventricular tachycardia may be classified by duration of RP interval compared to PR interval on ECG. Short RP interval SVT includes AVNRT and AVRT through a rapidly conducting accessory path. Long RP interval SVT includes atypical AVNRT, atrial tachycardia, and PJRT.

 

Persistent Junctional Reentrant Tachycardia

Persistent junctional reentrant tachycardia is a rare form of long RP tachycardia, accounting for approximately 1% of SVT in a study review of 21 patients.³ As with the patient in this case, PJRT usually presents in early childhood.³   In a recent review of 194 patients with PJRT, 57% were infants.⁴ The condition involves an accessory pathway most commonly located in the posterior-superior septal region; conduction involves a retrograde impulse through the decremental accessory pathway.⁵ On ECG, findings include a negative P wave in inferior leads, a long RP interval, and a 1:1 AV conduction.⁶

A long-term multicenter follow-up study of 32 patients showed that rates of tachycardia vary among patients, from 100 to 250 beats/minute.⁷ Tachycardia-induced cardiomyopathy (TIC), which is secondary to the incessant nature of tachycardia, may be present in up to 30% to 50% of patients.^3,8 In a recent multicenter study, PJRT was responsible for 23% of cases of TIC.⁹ Although the exact mechanism of this property is unknown, decremental conduction and unidirectional block of the accessory pathway appear to be contributing factors.⁶

Treatment

Adenosine is the initial drug of choice for narrow complex tachycardia with stable hemodynamic status and an available intravascular access.¹⁰ In a study evaluating the effectiveness of adenosine for managing SVT in the pediatric ED setting, it was more than 70% effective in cardioverting patients presumed to have SVT.¹¹ However, in PJRT, owing to the incessant pattern, adenosine may either terminate the tachycardia (causing asystole) or, as seen in this patient, convert tachycardia to sinus rhythm for only a few seconds.¹² Reinitiation of tachycardia in sinus beat without the need for a premature complex contributes to its incessant nature.¹³

In a multicenter study looking at clinical profile and outcome for PJRT, Vaksmann et al⁸ found a greater than 80% success rate in controlling the dysrhythmia with amiodarone and verapamil. For long-term management of tachyarrhythmia, medical therapy has been recommended in early childhood compared to older children in whom catheter ablation is an effective approach.⁷ Spontaneous resolution of PJRT has been documented but is rare.¹⁴

Conclusion

Pediatric cardiac emergencies require very specific treatment. As such, it is important that the emergency physician distinguish the different the types of tachyarrhythmias—especially in cases that do not respond to treatment with adenosine. In the pediatric patient, PJRT is a potentially life-threatening arrhythmia that requires a high index of suspicion. Clues to diagnosis include negative P waves in inferior leads, long RP interval, and 1:1 atrioventricular conduction.

Dr Fichadia is a fellow, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan. Dr Perez is a clinical instructor, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan.

CHICAGO – An experimental triple-drug regimen with or without ribavirin cured more than 90% of 724 previously untreated patients with hepatitis C genotype 1 who did not have cirrhosis.

And it was done without interferon.

Dr. Bruce R. Bacon called this oral regimen "revolutionary" in an interview during the annual Digestive Disease Week. Dr. Bacon is the James F. King Endowed Chair in Gastroenterology and a professor of medicine at St. Louis University. He was not involved in the study.

Hear his thoughts on treatment with ABT-450 with ritonavir, ombitasvir, and dasabuvir (known as the "three D" regimen) with or without ribavirin.

Dr. Bacon reported financial associations with AbbVie, which is developing the new drugs; Gilead Sciences; and Janssen Pharmaceuticals.

[email protected]

On Twitter @sherryboschert

CHICAGO – An experimental triple-drug regimen with or without ribavirin cured more than 90% of 724 previously untreated patients with hepatitis C genotype 1 who did not have cirrhosis.

And it was done without interferon.

Dr. Bruce R. Bacon called this oral regimen "revolutionary" in an interview during the annual Digestive Disease Week. Dr. Bacon is the James F. King Endowed Chair in Gastroenterology and a professor of medicine at St. Louis University. He was not involved in the study.

Hear his thoughts on treatment with ABT-450 with ritonavir, ombitasvir, and dasabuvir (known as the "three D" regimen) with or without ribavirin.

Dr. Bacon reported financial associations with AbbVie, which is developing the new drugs; Gilead Sciences; and Janssen Pharmaceuticals.

[email protected]

On Twitter @sherryboschert

CHICAGO – An experimental triple-drug regimen with or without ribavirin cured more than 90% of 724 previously untreated patients with hepatitis C genotype 1 who did not have cirrhosis.

And it was done without interferon.

Dr. Bruce R. Bacon called this oral regimen "revolutionary" in an interview during the annual Digestive Disease Week. Dr. Bacon is the James F. King Endowed Chair in Gastroenterology and a professor of medicine at St. Louis University. He was not involved in the study.

Hear his thoughts on treatment with ABT-450 with ritonavir, ombitasvir, and dasabuvir (known as the "three D" regimen) with or without ribavirin.

Dr. Bacon reported financial associations with AbbVie, which is developing the new drugs; Gilead Sciences; and Janssen Pharmaceuticals.

[email protected]

On Twitter @sherryboschert

Patients participating in occupational and sports-related activities requiring ascent to high elevations are at risk of developing a range of high-altitude illnesses. Prompt recognition and treatment are paramount to improving outcomes and preventing life-threatening sequelae. High-elevation locations are the setting of many recreational activities for outdoor enthusiasts. As such, illnesses associated with high altitude may be encountered by those summiting peaks, traveling by air, or working in flight medicine or as part of an emergency rescue team. The altitude syndromes discussed in this review are acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). While these conditions do not represent all altitude-related illnesses, they are the primary pathological processes for which physicians should be familiar when working with high-altitude populations.

Physiological Response to Altitude

A knowledge of the physiological response to altitude helps to understand altitude-related illness. The normal acclimatization response to high elevation involves an increase in alveolar ventilation, referred to as hypoxic ventilatory response (HVR). The HVR is initiated by the carotid body, which acts as a peripheral chemosensor. Over the first 2 weeks at elevation, an increased sensitivity to hypoxia leads to a rise in ventilation. This precipitates an increase in alveolar oxygen pressure and arterial oxygen concentration, and a decrease in arterial carbon dioxide. Cardiac output increases, ventilation perfusion-matching is improved, and pulmonary arterial pressure rises. Respiratory alkalosis develops secondary to this hyperventilation; as a compensatory response, increased excretion of bicarbonate by the kidneys occurs, leading to a normalization of pH, which peaks at about 7 days. These physiological changes result in hyperventilation, increased urinary output, periodic nighttime breathing, and dyspnea on exertion. Periodic nighttime breathing is characterized by periods of hyperpnea followed by apnea during sleep. The duration of apnea is commonly 3 to 10 seconds, but may last up to 15 seconds. These symptoms may be considered normal at elevations above 8,000 ft.

The Lake Louise Criteria

At the 1991 International Hypoxia Symposium in Alberta, Canada, the Lake Louise criteria regarding the diagnosis of altitude illness was developed and adopted.¹ This consensus statement provides definitions for AMS, HACE, and HAPE (Table 1). In addition to the definition criteria, a self-assessment scoring system, which includes a clinical assessment, was developed to assist in diagnosing high-altitude illness (Table 2).²

Acute Mountain Sickness

Acute mountain sickness comprises a constellation of symptoms caused by the atmospheric changes at elevations above approximately 2,500 m. It is the most common form of high-altitude illness, affecting 25% of travelers at moderate altitude and 50% to 85% above 4,000 m.³

Symptoms
The onset of symptoms (eg, headache, anorexia, nausea, vomiting, weakness) may occur at 2,000 m in the setting of rapid ascent—most commonly at 6 to 12 hours, but onset can range from 1 hour to 2 days after ascent. If symptoms begin after 3 days, other diagnoses should be considered. Symptoms of AMS are generally worse after the first night of sleep at elevation. On physical examination, vital signs are usually normal, though postural hypotension and tachycardia are possible. Oxygen saturation may be markedly decreased after rapid ascent, and chest auscultation may reveal rales in 20% of patients.⁴ Peripheral and facial edema may also be present. Funduscopic examination may show venous tortuosity and dilation, and retinal hemorrhage is common in ascents over 4,800 m.

© Shutterstock/sezer66

Differential Diagnosis
The differential diagnosis for AMS is broad and includes hypothermia, dehydration, exhaustion, subarachnoid hemorrhage, intracranial mass, carbon monoxide poisoning, alcohol hangover, intoxication, central nervous system infection and migraine. Risk factors for developing AMS are a previous history of altitude illness, rapid ascent, and lack of previous acclimatization. Interestingly, physical fitness does not protect a person from developing AMS.⁵

Mechanism of AMS
The true mechanism of AMS is uncertain, but it is clear that a fall in barometric pressure results in hypobaric hypoxia. This is thought to lead to an increased blood volume in the brain and increased cerebral blood flow, possibly precipitating an enlarged brain. A mechanism related to vasogenic edema has been proposed due to patients’ clinical improvement with dexamethasone therapy.⁶ Acute mountain sickness does appear to be related to overall fluid balance, as an increase in reninangiotensin, aldosterone, and antidiuretic hormone has been observed in patients with the condition. Elevation of these hormones is contrary to the appropriate physiological response of diuresis.

Treatment
Treatment of AMS begins with descent from elevation as soon as possible. Descent should be at least 500 m from the aggravating elevation. Patients should remain at least 1 to 2 days at this lower elevation before attempting reascent. If descent is not feasible, any further ascent should be delayed until symptoms have resolved.
     Dexamethasone. This glucocorticoid has been used clinically with good success, although the mechanism of action in unclear. The initial dose is 8 mg followed by 4 mg every 6 hours.³
     Acetazolamide. A carbonic anhydrase inhibitor, acetazolamide acts to temper symptoms by causing an acidosis that increases ventilation and prevents periodic breathing and hypoxia during sleep. The standard dose is 250 mg twice daily.³
    Oxygen. Supplemental oxygen provided at 1 to 2 L/min via nasal cannula for 12 to 24 hours may help to improve symptoms. A portable hyperbaric oxygen (HBO) bag (eg, a Gamow bag) can be used to create an effective altitude of approximately 1,500 to 2,000 m inside the bag. The patient is placed completely within the bag, the zipper is sealed shut, and the bag is inflated with a foot pump. Treatment in such a chamber can be provided in 1-hour increments and repeated as needed. However, if descent is possible, use of the HBO chamber should not prevent or delay descent.
     Ibuprofen. Compared to placebo, studies have shown ibuprofen 600 mg three times a day reduces the severity of AMS.⁷

Prevention
Strategies to prevent AMS are similar to those used to treat the condition. These include gradual ascent and prophylactic drug therapy.
     Gradual Ascent. Gradual ascent is the primary strategy to prevent AMS. At altitudes above 3,000 m, each subsequent night should not be spent at an elevation 300 m higher than the previous night.
     Acetazolamide. Pretreatment with acetazolamide is indicated for patients with a history of altitude illness or who anticipate an abrupt ascent (eg, rescue workers). Acetazolamide has been shown in multiple studies to be effective in the prevention of AMS.⁸ Adverse side effects of acetazolamide include paresthesias and increased urinary frequency; the drug may also make carbonated beverages taste flat. The preventive dose is 125 mg twice daily, and should be started the day before ascent.
     Dexamethasone. In addition to treating AMS, dexamethasone may be taken as a preventive in doses of 2 mg every 6 hours or 4 mg twice daily.³ However, unlike acetazolamide, which acts to facilitate acclimatization, dexamethasone only prevents symptoms. Thus, cessation of the drug can result in rebound AMS symptoms, and prolonged use can result in adrenal suppression.³ Therefore, it should not be used for more than 10 days.
     Sumatriptan and Gabapentin. In recent studies, sumatriptan and gabapentin haven shown benefit in preventing AMS, ^9,10 but further study is needed before either of these drugs can be recommended.
     Ginkgo Biloba. While ginkgo biloba has been touted as an effective preventive treatment, studies have shown no benefit to its use.⁸
    Ibuprofen. ibuprofen 600 mg three times daily can be initiated the day prior to ascent, and has been shown to decrease the incidence of AMS.⁷

 

High-Altitude Cerebral Edema

High-altitude cerebral edema, a condition that can be considered on a continuum with AMS, is hallmarked by progressive neurological symptoms. It is defined by either the presence of a change in mental status and/or ataxia in a person with AMS, or the presence of both mental status changes and ataxia in a person without AMS. Clinical signs are truncal ataxia, hallucinations, confusion, vomiting, decreased activity, mild fever, upper motor neuronal signs, stupor, or coma.⁵ Development of HACE usually requires at least 2 days of altitudes above 4000 m.⁵

Mechanism of HACE
The exact mechanism of HACE is unclear. Magnetic resonance imaging of patients with the condition demonstrates cerebral edema primarily localized to the corpus callosum.¹¹ These findings suggest an increased permeability in the blood-brain barrier, leading to vasogenic cerebral edema. Cases of death associated with HACE are the result of herniation. Fortunately, if the condition is recognized promptly and appropriate management is instituted, most patients will recover without permanent deficits.

Treatment
Current recommendations for treating HACE are similar to treatment strategies for AMS.
    Descent. A therapeutic priority, descent may prove challenging as the patient may be ataxic, have altered mental status, and have difficulty facilitating his or her own descent.
     Oxygen. A portable HBO bag can be used to simulate descent until evacuation is possible. Supplemental oxygen should be applied immediately.
    Dexamethasone. In treating HACE, dexamethasone may be administered at a loading dose of 8 mg, followed by 4 mg every 6 hours.³
     Airway Management. If the patient has significantly altered mental status, appropriate airway management must be initiated.

High-Altitude Pulmonary Edema

The most common cause of death from altitude illness is HAPE,¹² a form of noncardiogenic pulmonary edema. This condition generally occurs at elevations above 3,000 m. Symptoms begin 2 to 5 days after ascent and progress in a typical pattern. A patient will initially experience a nonproductive cough and dyspnea at rest. The dyspnea worsens, and the cough becomes productive of pink, frothy sputum. Without medical intervention, lethargy, coma, and death may follow.

Symptoms of HAPE generally worsen following a night of sleep at elevation. Physical examination reveals crackles, tachycardia, tachypnea, and hypoxia. Diagnosis requires at least two of the following signs:

• Crackles or wheezing in at least one lung field
• Central cyanosis
• Tachypnea
• Tachycardia.

In addition to the above signs, at least two of the following symptoms must also be present:

• Dyspnea at rest
• Cough
• Weakness or decreased exercise performance
• Chest tightness
• Congestion.

Chest X-ray typically reveals patchy opacities at varying locations (Figure 2). There are often infiltrates in the right middle lobe. Ultrasound has been used to facilitate the diagnosis of HAPE in the field.¹³ The “comet-tail” sign is a term used to describe echogenic patterns in the lung as a result of increased lymphatic flow (Figure 3). This sign, if seen in the clinical setting of HAPE, may aid in the diagnosis and monitoring of treatment efficacy.¹³

Mechanism of HAPE
The mechanism of HAPE is better understood than that of AMS and HACE. In HAPE, high microvascular pressures in the lungs lead to elevated pulmonary vascular resistance and pulmonary artery pressure. Pulmonary edema ensues, but left ventricular function is preserved. Patients with a naturally low HVR, high pulmonary artery pressures at rest, preexisting pulmonary hypertension, or a previous history of HAPE are predisposed to developing the condition. Risk factors include heavy exertion, rapid ascent, cold, salt ingestion, and sleeping medications.

© Shutterstock/Telegin Sergey

Treatment
Decent and warming of the patient as soon as possible, along with treatment outlined below, are essential.
     Oxygen. Treatment of HAPE begins with supplemental oxygen to immediately lower pulmonary artery pressure. Oxygen should initially be administered at 4 to 6 L/min; if the patient improves clinically and can maintain oxygen saturations greater than 90%, oxygen may be decreased with a goal to maintain saturation above 90%.
     Nifedipine. Following oxygen, descent, and warming, nifedipine can be used as an adjunctive therapy. The treatment dose for HAPE is 20 to 30 mg of the sustained release form every 12 hours.³
     Salmeterol/Albuterol and Expiratory Positive Airway Pressure. The oral inhalers salmeterol or albuterol may be used for bronchodilation; however, there is little evidence to support their effectiveness in HAPE. Ventilation with expiratory positive airway pressure can be employed if available.

Prevention
For patients with a predisposition to HAPE, preventive measures should be considered prior to ascent. As with all forms of altitude illness, gradual ascent is the most effective prevention method available.
     Phosphodiesterase Inhibitors. Phosphodiesterase inhibitors act via pulmonary vasodilation to prevent HAPE in some patients. Tadalafil at a dose of 10 mg twice daily or 20 mg once daily has been shown to reduce the incidence of HAPE.¹⁴ Alternatively, sildenafil 50 mg three times daily may be used.
     Acetazolamide and β-Agonists. Although both acetazolamide and β-agonists such as albuterol have been theorized to aid in preventing HAPE, this has not been proven.¹⁵

 

Conclusion

Clinically, high-altitude illnesses range from subtle symptoms to severe, life threatening disease. Knowledge of these disease processes and clinical presentation prior to travel or work in a high-altitude setting is essential. Rapid recognition of symptoms and prompt, appropriate interventions, such as descent when necessary, can significantly improve the outcomes of these conditions.

Dr Haroutunian is an emergency physician, department of emergency medicine, Exempla St Joseph Hospital, Denver, Colorado. Dr Bono is professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk.

Patients participating in occupational and sports-related activities requiring ascent to high elevations are at risk of developing a range of high-altitude illnesses. Prompt recognition and treatment are paramount to improving outcomes and preventing life-threatening sequelae. High-elevation locations are the setting of many recreational activities for outdoor enthusiasts. As such, illnesses associated with high altitude may be encountered by those summiting peaks, traveling by air, or working in flight medicine or as part of an emergency rescue team. The altitude syndromes discussed in this review are acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). While these conditions do not represent all altitude-related illnesses, they are the primary pathological processes for which physicians should be familiar when working with high-altitude populations.

Physiological Response to Altitude

A knowledge of the physiological response to altitude helps to understand altitude-related illness. The normal acclimatization response to high elevation involves an increase in alveolar ventilation, referred to as hypoxic ventilatory response (HVR). The HVR is initiated by the carotid body, which acts as a peripheral chemosensor. Over the first 2 weeks at elevation, an increased sensitivity to hypoxia leads to a rise in ventilation. This precipitates an increase in alveolar oxygen pressure and arterial oxygen concentration, and a decrease in arterial carbon dioxide. Cardiac output increases, ventilation perfusion-matching is improved, and pulmonary arterial pressure rises. Respiratory alkalosis develops secondary to this hyperventilation; as a compensatory response, increased excretion of bicarbonate by the kidneys occurs, leading to a normalization of pH, which peaks at about 7 days. These physiological changes result in hyperventilation, increased urinary output, periodic nighttime breathing, and dyspnea on exertion. Periodic nighttime breathing is characterized by periods of hyperpnea followed by apnea during sleep. The duration of apnea is commonly 3 to 10 seconds, but may last up to 15 seconds. These symptoms may be considered normal at elevations above 8,000 ft.

The Lake Louise Criteria

At the 1991 International Hypoxia Symposium in Alberta, Canada, the Lake Louise criteria regarding the diagnosis of altitude illness was developed and adopted.¹ This consensus statement provides definitions for AMS, HACE, and HAPE (Table 1). In addition to the definition criteria, a self-assessment scoring system, which includes a clinical assessment, was developed to assist in diagnosing high-altitude illness (Table 2).²

Acute Mountain Sickness

Acute mountain sickness comprises a constellation of symptoms caused by the atmospheric changes at elevations above approximately 2,500 m. It is the most common form of high-altitude illness, affecting 25% of travelers at moderate altitude and 50% to 85% above 4,000 m.³

Symptoms
The onset of symptoms (eg, headache, anorexia, nausea, vomiting, weakness) may occur at 2,000 m in the setting of rapid ascent—most commonly at 6 to 12 hours, but onset can range from 1 hour to 2 days after ascent. If symptoms begin after 3 days, other diagnoses should be considered. Symptoms of AMS are generally worse after the first night of sleep at elevation. On physical examination, vital signs are usually normal, though postural hypotension and tachycardia are possible. Oxygen saturation may be markedly decreased after rapid ascent, and chest auscultation may reveal rales in 20% of patients.⁴ Peripheral and facial edema may also be present. Funduscopic examination may show venous tortuosity and dilation, and retinal hemorrhage is common in ascents over 4,800 m.

© Shutterstock/sezer66

Differential Diagnosis
The differential diagnosis for AMS is broad and includes hypothermia, dehydration, exhaustion, subarachnoid hemorrhage, intracranial mass, carbon monoxide poisoning, alcohol hangover, intoxication, central nervous system infection and migraine. Risk factors for developing AMS are a previous history of altitude illness, rapid ascent, and lack of previous acclimatization. Interestingly, physical fitness does not protect a person from developing AMS.⁵

Mechanism of AMS
The true mechanism of AMS is uncertain, but it is clear that a fall in barometric pressure results in hypobaric hypoxia. This is thought to lead to an increased blood volume in the brain and increased cerebral blood flow, possibly precipitating an enlarged brain. A mechanism related to vasogenic edema has been proposed due to patients’ clinical improvement with dexamethasone therapy.⁶ Acute mountain sickness does appear to be related to overall fluid balance, as an increase in reninangiotensin, aldosterone, and antidiuretic hormone has been observed in patients with the condition. Elevation of these hormones is contrary to the appropriate physiological response of diuresis.

Treatment
Treatment of AMS begins with descent from elevation as soon as possible. Descent should be at least 500 m from the aggravating elevation. Patients should remain at least 1 to 2 days at this lower elevation before attempting reascent. If descent is not feasible, any further ascent should be delayed until symptoms have resolved.
     Dexamethasone. This glucocorticoid has been used clinically with good success, although the mechanism of action in unclear. The initial dose is 8 mg followed by 4 mg every 6 hours.³
     Acetazolamide. A carbonic anhydrase inhibitor, acetazolamide acts to temper symptoms by causing an acidosis that increases ventilation and prevents periodic breathing and hypoxia during sleep. The standard dose is 250 mg twice daily.³
    Oxygen. Supplemental oxygen provided at 1 to 2 L/min via nasal cannula for 12 to 24 hours may help to improve symptoms. A portable hyperbaric oxygen (HBO) bag (eg, a Gamow bag) can be used to create an effective altitude of approximately 1,500 to 2,000 m inside the bag. The patient is placed completely within the bag, the zipper is sealed shut, and the bag is inflated with a foot pump. Treatment in such a chamber can be provided in 1-hour increments and repeated as needed. However, if descent is possible, use of the HBO chamber should not prevent or delay descent.
     Ibuprofen. Compared to placebo, studies have shown ibuprofen 600 mg three times a day reduces the severity of AMS.⁷

Prevention
Strategies to prevent AMS are similar to those used to treat the condition. These include gradual ascent and prophylactic drug therapy.
     Gradual Ascent. Gradual ascent is the primary strategy to prevent AMS. At altitudes above 3,000 m, each subsequent night should not be spent at an elevation 300 m higher than the previous night.
     Acetazolamide. Pretreatment with acetazolamide is indicated for patients with a history of altitude illness or who anticipate an abrupt ascent (eg, rescue workers). Acetazolamide has been shown in multiple studies to be effective in the prevention of AMS.⁸ Adverse side effects of acetazolamide include paresthesias and increased urinary frequency; the drug may also make carbonated beverages taste flat. The preventive dose is 125 mg twice daily, and should be started the day before ascent.
     Dexamethasone. In addition to treating AMS, dexamethasone may be taken as a preventive in doses of 2 mg every 6 hours or 4 mg twice daily.³ However, unlike acetazolamide, which acts to facilitate acclimatization, dexamethasone only prevents symptoms. Thus, cessation of the drug can result in rebound AMS symptoms, and prolonged use can result in adrenal suppression.³ Therefore, it should not be used for more than 10 days.
     Sumatriptan and Gabapentin. In recent studies, sumatriptan and gabapentin haven shown benefit in preventing AMS, ^9,10 but further study is needed before either of these drugs can be recommended.
     Ginkgo Biloba. While ginkgo biloba has been touted as an effective preventive treatment, studies have shown no benefit to its use.⁸
    Ibuprofen. ibuprofen 600 mg three times daily can be initiated the day prior to ascent, and has been shown to decrease the incidence of AMS.⁷

 

High-Altitude Cerebral Edema

High-altitude cerebral edema, a condition that can be considered on a continuum with AMS, is hallmarked by progressive neurological symptoms. It is defined by either the presence of a change in mental status and/or ataxia in a person with AMS, or the presence of both mental status changes and ataxia in a person without AMS. Clinical signs are truncal ataxia, hallucinations, confusion, vomiting, decreased activity, mild fever, upper motor neuronal signs, stupor, or coma.⁵ Development of HACE usually requires at least 2 days of altitudes above 4000 m.⁵

Mechanism of HACE
The exact mechanism of HACE is unclear. Magnetic resonance imaging of patients with the condition demonstrates cerebral edema primarily localized to the corpus callosum.¹¹ These findings suggest an increased permeability in the blood-brain barrier, leading to vasogenic cerebral edema. Cases of death associated with HACE are the result of herniation. Fortunately, if the condition is recognized promptly and appropriate management is instituted, most patients will recover without permanent deficits.

Treatment
Current recommendations for treating HACE are similar to treatment strategies for AMS.
    Descent. A therapeutic priority, descent may prove challenging as the patient may be ataxic, have altered mental status, and have difficulty facilitating his or her own descent.
     Oxygen. A portable HBO bag can be used to simulate descent until evacuation is possible. Supplemental oxygen should be applied immediately.
    Dexamethasone. In treating HACE, dexamethasone may be administered at a loading dose of 8 mg, followed by 4 mg every 6 hours.³
     Airway Management. If the patient has significantly altered mental status, appropriate airway management must be initiated.

High-Altitude Pulmonary Edema

The most common cause of death from altitude illness is HAPE,¹² a form of noncardiogenic pulmonary edema. This condition generally occurs at elevations above 3,000 m. Symptoms begin 2 to 5 days after ascent and progress in a typical pattern. A patient will initially experience a nonproductive cough and dyspnea at rest. The dyspnea worsens, and the cough becomes productive of pink, frothy sputum. Without medical intervention, lethargy, coma, and death may follow.

Symptoms of HAPE generally worsen following a night of sleep at elevation. Physical examination reveals crackles, tachycardia, tachypnea, and hypoxia. Diagnosis requires at least two of the following signs:

• Crackles or wheezing in at least one lung field
• Central cyanosis
• Tachypnea
• Tachycardia.

In addition to the above signs, at least two of the following symptoms must also be present:

• Dyspnea at rest
• Cough
• Weakness or decreased exercise performance
• Chest tightness
• Congestion.

Chest X-ray typically reveals patchy opacities at varying locations (Figure 2). There are often infiltrates in the right middle lobe. Ultrasound has been used to facilitate the diagnosis of HAPE in the field.¹³ The “comet-tail” sign is a term used to describe echogenic patterns in the lung as a result of increased lymphatic flow (Figure 3). This sign, if seen in the clinical setting of HAPE, may aid in the diagnosis and monitoring of treatment efficacy.¹³

Mechanism of HAPE
The mechanism of HAPE is better understood than that of AMS and HACE. In HAPE, high microvascular pressures in the lungs lead to elevated pulmonary vascular resistance and pulmonary artery pressure. Pulmonary edema ensues, but left ventricular function is preserved. Patients with a naturally low HVR, high pulmonary artery pressures at rest, preexisting pulmonary hypertension, or a previous history of HAPE are predisposed to developing the condition. Risk factors include heavy exertion, rapid ascent, cold, salt ingestion, and sleeping medications.

© Shutterstock/Telegin Sergey

Treatment
Decent and warming of the patient as soon as possible, along with treatment outlined below, are essential.
     Oxygen. Treatment of HAPE begins with supplemental oxygen to immediately lower pulmonary artery pressure. Oxygen should initially be administered at 4 to 6 L/min; if the patient improves clinically and can maintain oxygen saturations greater than 90%, oxygen may be decreased with a goal to maintain saturation above 90%.
     Nifedipine. Following oxygen, descent, and warming, nifedipine can be used as an adjunctive therapy. The treatment dose for HAPE is 20 to 30 mg of the sustained release form every 12 hours.³
     Salmeterol/Albuterol and Expiratory Positive Airway Pressure. The oral inhalers salmeterol or albuterol may be used for bronchodilation; however, there is little evidence to support their effectiveness in HAPE. Ventilation with expiratory positive airway pressure can be employed if available.

Prevention
For patients with a predisposition to HAPE, preventive measures should be considered prior to ascent. As with all forms of altitude illness, gradual ascent is the most effective prevention method available.
     Phosphodiesterase Inhibitors. Phosphodiesterase inhibitors act via pulmonary vasodilation to prevent HAPE in some patients. Tadalafil at a dose of 10 mg twice daily or 20 mg once daily has been shown to reduce the incidence of HAPE.¹⁴ Alternatively, sildenafil 50 mg three times daily may be used.
     Acetazolamide and β-Agonists. Although both acetazolamide and β-agonists such as albuterol have been theorized to aid in preventing HAPE, this has not been proven.¹⁵

 

Conclusion

Clinically, high-altitude illnesses range from subtle symptoms to severe, life threatening disease. Knowledge of these disease processes and clinical presentation prior to travel or work in a high-altitude setting is essential. Rapid recognition of symptoms and prompt, appropriate interventions, such as descent when necessary, can significantly improve the outcomes of these conditions.

Dr Haroutunian is an emergency physician, department of emergency medicine, Exempla St Joseph Hospital, Denver, Colorado. Dr Bono is professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk.

Patients participating in occupational and sports-related activities requiring ascent to high elevations are at risk of developing a range of high-altitude illnesses. Prompt recognition and treatment are paramount to improving outcomes and preventing life-threatening sequelae. High-elevation locations are the setting of many recreational activities for outdoor enthusiasts. As such, illnesses associated with high altitude may be encountered by those summiting peaks, traveling by air, or working in flight medicine or as part of an emergency rescue team. The altitude syndromes discussed in this review are acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). While these conditions do not represent all altitude-related illnesses, they are the primary pathological processes for which physicians should be familiar when working with high-altitude populations.

Physiological Response to Altitude

A knowledge of the physiological response to altitude helps to understand altitude-related illness. The normal acclimatization response to high elevation involves an increase in alveolar ventilation, referred to as hypoxic ventilatory response (HVR). The HVR is initiated by the carotid body, which acts as a peripheral chemosensor. Over the first 2 weeks at elevation, an increased sensitivity to hypoxia leads to a rise in ventilation. This precipitates an increase in alveolar oxygen pressure and arterial oxygen concentration, and a decrease in arterial carbon dioxide. Cardiac output increases, ventilation perfusion-matching is improved, and pulmonary arterial pressure rises. Respiratory alkalosis develops secondary to this hyperventilation; as a compensatory response, increased excretion of bicarbonate by the kidneys occurs, leading to a normalization of pH, which peaks at about 7 days. These physiological changes result in hyperventilation, increased urinary output, periodic nighttime breathing, and dyspnea on exertion. Periodic nighttime breathing is characterized by periods of hyperpnea followed by apnea during sleep. The duration of apnea is commonly 3 to 10 seconds, but may last up to 15 seconds. These symptoms may be considered normal at elevations above 8,000 ft.

The Lake Louise Criteria

At the 1991 International Hypoxia Symposium in Alberta, Canada, the Lake Louise criteria regarding the diagnosis of altitude illness was developed and adopted.¹ This consensus statement provides definitions for AMS, HACE, and HAPE (Table 1). In addition to the definition criteria, a self-assessment scoring system, which includes a clinical assessment, was developed to assist in diagnosing high-altitude illness (Table 2).²

Acute Mountain Sickness

Acute mountain sickness comprises a constellation of symptoms caused by the atmospheric changes at elevations above approximately 2,500 m. It is the most common form of high-altitude illness, affecting 25% of travelers at moderate altitude and 50% to 85% above 4,000 m.³

Symptoms
The onset of symptoms (eg, headache, anorexia, nausea, vomiting, weakness) may occur at 2,000 m in the setting of rapid ascent—most commonly at 6 to 12 hours, but onset can range from 1 hour to 2 days after ascent. If symptoms begin after 3 days, other diagnoses should be considered. Symptoms of AMS are generally worse after the first night of sleep at elevation. On physical examination, vital signs are usually normal, though postural hypotension and tachycardia are possible. Oxygen saturation may be markedly decreased after rapid ascent, and chest auscultation may reveal rales in 20% of patients.⁴ Peripheral and facial edema may also be present. Funduscopic examination may show venous tortuosity and dilation, and retinal hemorrhage is common in ascents over 4,800 m.

© Shutterstock/sezer66

Differential Diagnosis
The differential diagnosis for AMS is broad and includes hypothermia, dehydration, exhaustion, subarachnoid hemorrhage, intracranial mass, carbon monoxide poisoning, alcohol hangover, intoxication, central nervous system infection and migraine. Risk factors for developing AMS are a previous history of altitude illness, rapid ascent, and lack of previous acclimatization. Interestingly, physical fitness does not protect a person from developing AMS.⁵

Mechanism of AMS
The true mechanism of AMS is uncertain, but it is clear that a fall in barometric pressure results in hypobaric hypoxia. This is thought to lead to an increased blood volume in the brain and increased cerebral blood flow, possibly precipitating an enlarged brain. A mechanism related to vasogenic edema has been proposed due to patients’ clinical improvement with dexamethasone therapy.⁶ Acute mountain sickness does appear to be related to overall fluid balance, as an increase in reninangiotensin, aldosterone, and antidiuretic hormone has been observed in patients with the condition. Elevation of these hormones is contrary to the appropriate physiological response of diuresis.

Treatment
Treatment of AMS begins with descent from elevation as soon as possible. Descent should be at least 500 m from the aggravating elevation. Patients should remain at least 1 to 2 days at this lower elevation before attempting reascent. If descent is not feasible, any further ascent should be delayed until symptoms have resolved.
     Dexamethasone. This glucocorticoid has been used clinically with good success, although the mechanism of action in unclear. The initial dose is 8 mg followed by 4 mg every 6 hours.³
     Acetazolamide. A carbonic anhydrase inhibitor, acetazolamide acts to temper symptoms by causing an acidosis that increases ventilation and prevents periodic breathing and hypoxia during sleep. The standard dose is 250 mg twice daily.³
    Oxygen. Supplemental oxygen provided at 1 to 2 L/min via nasal cannula for 12 to 24 hours may help to improve symptoms. A portable hyperbaric oxygen (HBO) bag (eg, a Gamow bag) can be used to create an effective altitude of approximately 1,500 to 2,000 m inside the bag. The patient is placed completely within the bag, the zipper is sealed shut, and the bag is inflated with a foot pump. Treatment in such a chamber can be provided in 1-hour increments and repeated as needed. However, if descent is possible, use of the HBO chamber should not prevent or delay descent.
     Ibuprofen. Compared to placebo, studies have shown ibuprofen 600 mg three times a day reduces the severity of AMS.⁷

Prevention
Strategies to prevent AMS are similar to those used to treat the condition. These include gradual ascent and prophylactic drug therapy.
     Gradual Ascent. Gradual ascent is the primary strategy to prevent AMS. At altitudes above 3,000 m, each subsequent night should not be spent at an elevation 300 m higher than the previous night.
     Acetazolamide. Pretreatment with acetazolamide is indicated for patients with a history of altitude illness or who anticipate an abrupt ascent (eg, rescue workers). Acetazolamide has been shown in multiple studies to be effective in the prevention of AMS.⁸ Adverse side effects of acetazolamide include paresthesias and increased urinary frequency; the drug may also make carbonated beverages taste flat. The preventive dose is 125 mg twice daily, and should be started the day before ascent.
     Dexamethasone. In addition to treating AMS, dexamethasone may be taken as a preventive in doses of 2 mg every 6 hours or 4 mg twice daily.³ However, unlike acetazolamide, which acts to facilitate acclimatization, dexamethasone only prevents symptoms. Thus, cessation of the drug can result in rebound AMS symptoms, and prolonged use can result in adrenal suppression.³ Therefore, it should not be used for more than 10 days.
     Sumatriptan and Gabapentin. In recent studies, sumatriptan and gabapentin haven shown benefit in preventing AMS, ^9,10 but further study is needed before either of these drugs can be recommended.
     Ginkgo Biloba. While ginkgo biloba has been touted as an effective preventive treatment, studies have shown no benefit to its use.⁸
    Ibuprofen. ibuprofen 600 mg three times daily can be initiated the day prior to ascent, and has been shown to decrease the incidence of AMS.⁷

 

High-Altitude Cerebral Edema

High-altitude cerebral edema, a condition that can be considered on a continuum with AMS, is hallmarked by progressive neurological symptoms. It is defined by either the presence of a change in mental status and/or ataxia in a person with AMS, or the presence of both mental status changes and ataxia in a person without AMS. Clinical signs are truncal ataxia, hallucinations, confusion, vomiting, decreased activity, mild fever, upper motor neuronal signs, stupor, or coma.⁵ Development of HACE usually requires at least 2 days of altitudes above 4000 m.⁵

Mechanism of HACE
The exact mechanism of HACE is unclear. Magnetic resonance imaging of patients with the condition demonstrates cerebral edema primarily localized to the corpus callosum.¹¹ These findings suggest an increased permeability in the blood-brain barrier, leading to vasogenic cerebral edema. Cases of death associated with HACE are the result of herniation. Fortunately, if the condition is recognized promptly and appropriate management is instituted, most patients will recover without permanent deficits.

Treatment
Current recommendations for treating HACE are similar to treatment strategies for AMS.
    Descent. A therapeutic priority, descent may prove challenging as the patient may be ataxic, have altered mental status, and have difficulty facilitating his or her own descent.
     Oxygen. A portable HBO bag can be used to simulate descent until evacuation is possible. Supplemental oxygen should be applied immediately.
    Dexamethasone. In treating HACE, dexamethasone may be administered at a loading dose of 8 mg, followed by 4 mg every 6 hours.³
     Airway Management. If the patient has significantly altered mental status, appropriate airway management must be initiated.

High-Altitude Pulmonary Edema

The most common cause of death from altitude illness is HAPE,¹² a form of noncardiogenic pulmonary edema. This condition generally occurs at elevations above 3,000 m. Symptoms begin 2 to 5 days after ascent and progress in a typical pattern. A patient will initially experience a nonproductive cough and dyspnea at rest. The dyspnea worsens, and the cough becomes productive of pink, frothy sputum. Without medical intervention, lethargy, coma, and death may follow.

Symptoms of HAPE generally worsen following a night of sleep at elevation. Physical examination reveals crackles, tachycardia, tachypnea, and hypoxia. Diagnosis requires at least two of the following signs:

• Crackles or wheezing in at least one lung field
• Central cyanosis
• Tachypnea
• Tachycardia.

In addition to the above signs, at least two of the following symptoms must also be present:

• Dyspnea at rest
• Cough
• Weakness or decreased exercise performance
• Chest tightness
• Congestion.

Chest X-ray typically reveals patchy opacities at varying locations (Figure 2). There are often infiltrates in the right middle lobe. Ultrasound has been used to facilitate the diagnosis of HAPE in the field.¹³ The “comet-tail” sign is a term used to describe echogenic patterns in the lung as a result of increased lymphatic flow (Figure 3). This sign, if seen in the clinical setting of HAPE, may aid in the diagnosis and monitoring of treatment efficacy.¹³

Mechanism of HAPE
The mechanism of HAPE is better understood than that of AMS and HACE. In HAPE, high microvascular pressures in the lungs lead to elevated pulmonary vascular resistance and pulmonary artery pressure. Pulmonary edema ensues, but left ventricular function is preserved. Patients with a naturally low HVR, high pulmonary artery pressures at rest, preexisting pulmonary hypertension, or a previous history of HAPE are predisposed to developing the condition. Risk factors include heavy exertion, rapid ascent, cold, salt ingestion, and sleeping medications.

© Shutterstock/Telegin Sergey

Treatment
Decent and warming of the patient as soon as possible, along with treatment outlined below, are essential.
     Oxygen. Treatment of HAPE begins with supplemental oxygen to immediately lower pulmonary artery pressure. Oxygen should initially be administered at 4 to 6 L/min; if the patient improves clinically and can maintain oxygen saturations greater than 90%, oxygen may be decreased with a goal to maintain saturation above 90%.
     Nifedipine. Following oxygen, descent, and warming, nifedipine can be used as an adjunctive therapy. The treatment dose for HAPE is 20 to 30 mg of the sustained release form every 12 hours.³
     Salmeterol/Albuterol and Expiratory Positive Airway Pressure. The oral inhalers salmeterol or albuterol may be used for bronchodilation; however, there is little evidence to support their effectiveness in HAPE. Ventilation with expiratory positive airway pressure can be employed if available.

Prevention
For patients with a predisposition to HAPE, preventive measures should be considered prior to ascent. As with all forms of altitude illness, gradual ascent is the most effective prevention method available.
     Phosphodiesterase Inhibitors. Phosphodiesterase inhibitors act via pulmonary vasodilation to prevent HAPE in some patients. Tadalafil at a dose of 10 mg twice daily or 20 mg once daily has been shown to reduce the incidence of HAPE.¹⁴ Alternatively, sildenafil 50 mg three times daily may be used.
     Acetazolamide and β-Agonists. Although both acetazolamide and β-agonists such as albuterol have been theorized to aid in preventing HAPE, this has not been proven.¹⁵

 

Conclusion

Clinically, high-altitude illnesses range from subtle symptoms to severe, life threatening disease. Knowledge of these disease processes and clinical presentation prior to travel or work in a high-altitude setting is essential. Rapid recognition of symptoms and prompt, appropriate interventions, such as descent when necessary, can significantly improve the outcomes of these conditions.

Dr Haroutunian is an emergency physician, department of emergency medicine, Exempla St Joseph Hospital, Denver, Colorado. Dr Bono is professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk.

A 25-year-old man with no significant past medical history presented with low-back pain that radiated down into his right thigh. The patient stated the pain began 1 week earlier when he was lifting weights and had increased in severity to the point where he was no longer able to walk or stand up straight. He had taken nonprescription nonsteroidal anti-inflammatory drugs but received no significant relief.

Radiographs of the lumbosacral spine were obtained; representative anteroposterior (AP) and lateral images are shown above (Figures 1 and 2).

The lateral view of the lumbar spine demonstrates mild anterolisthesis of L5 on S1 with the posterior cortex of L5 (white arrow, Figure 3) anterior to the posterior cortex of S1 (red arrow, Figure 3). Normally, the posterior cortices of the adjacent vertebral bodies should align. Lucency is also noted in the region of the pars interarticularis (white asterisk, Figure 3). The combination of anterolisthesis and this lucency in a young patient suggests the diagnosis of spondylolysis (pars defect).

Spondylolysis is a defect in the pars interarticularis of the vertebral arch and most commonly affects the lowest lumbar vertebrae, L5. Spondylolysis may be unilateral or bilateral. Bilateral lumbar spondylolysis can result in spondylolisthesis and instability, leading to debilitating low-back pain and neurological deficits. While the prevalence of spondylolysis is about 3% to 10% in the general population, it is more common in males than females, with a ratio of 2:1; the condition is also more prevalent in Eskimo populations (as high as 50%) and in white compared to black populations. Risk factors include a family history of spondylolysis, spina bifida occulta, and Scheuermann kyphosis.¹

The pathophysiology of spondylolysis is still uncertain. Two theories have been proposed—underlying dysplastic pars interarticularis versus repetitive microtrauma resulting in stress factors are the two proposed underlying mechanism. If patients are genetically predisposed, underlying dysplasia probably contributes to the pathology, while microtrauma triggers the actual defect.² Most patients respond well with conservative management.
When evaluating for spondylolysis, AP, lateral, 45-degree right and left oblique views, and collimated lateral views of the lumbosacral spine should be obtained. With this five-view study, up to 96.5% of pars defect can be identified.

In the general population, if spondylolysis is suspected and radiographs are negative, magnetic resonance imaging, computed tomography, and/or single-photon emission computed tomography bone scintigraphy can be used for further evaluation.^4,5 In this case, the diagnosis was made based on radiographic imaging, and the patient was discharged with a scheduled follow-up with an orthopedic surgeon.

Dr Salama is a resident of radiology, resident of radiology, New York-Presbyterian Hospital/Weill Cornell Medical Center, New York. Dr Belfi is an assistant professor of radiology, Weill Cornell Medical College New York; and an assistant attending radiologist, New York-Presbyterian Hospital/Weill Cornell Medical Center, New York. Dr Hentel is an associate professor of clinical radiology, Weill Cornell Medical College, New York. He is also chief of emergency/musculoskeletal imaging and executive vice-chairman for the department of radiology, New York-Presbyterian Hospital/Weill Cornell Medical Center. He is associate editor, imaging, of the EMERGENCY MEDICINE editorial board.

A 25-year-old man with no significant past medical history presented with low-back pain that radiated down into his right thigh. The patient stated the pain began 1 week earlier when he was lifting weights and had increased in severity to the point where he was no longer able to walk or stand up straight. He had taken nonprescription nonsteroidal anti-inflammatory drugs but received no significant relief.

Radiographs of the lumbosacral spine were obtained; representative anteroposterior (AP) and lateral images are shown above (Figures 1 and 2).

The lateral view of the lumbar spine demonstrates mild anterolisthesis of L5 on S1 with the posterior cortex of L5 (white arrow, Figure 3) anterior to the posterior cortex of S1 (red arrow, Figure 3). Normally, the posterior cortices of the adjacent vertebral bodies should align. Lucency is also noted in the region of the pars interarticularis (white asterisk, Figure 3). The combination of anterolisthesis and this lucency in a young patient suggests the diagnosis of spondylolysis (pars defect).

Spondylolysis is a defect in the pars interarticularis of the vertebral arch and most commonly affects the lowest lumbar vertebrae, L5. Spondylolysis may be unilateral or bilateral. Bilateral lumbar spondylolysis can result in spondylolisthesis and instability, leading to debilitating low-back pain and neurological deficits. While the prevalence of spondylolysis is about 3% to 10% in the general population, it is more common in males than females, with a ratio of 2:1; the condition is also more prevalent in Eskimo populations (as high as 50%) and in white compared to black populations. Risk factors include a family history of spondylolysis, spina bifida occulta, and Scheuermann kyphosis.¹

The pathophysiology of spondylolysis is still uncertain. Two theories have been proposed—underlying dysplastic pars interarticularis versus repetitive microtrauma resulting in stress factors are the two proposed underlying mechanism. If patients are genetically predisposed, underlying dysplasia probably contributes to the pathology, while microtrauma triggers the actual defect.² Most patients respond well with conservative management.
When evaluating for spondylolysis, AP, lateral, 45-degree right and left oblique views, and collimated lateral views of the lumbosacral spine should be obtained. With this five-view study, up to 96.5% of pars defect can be identified.

In the general population, if spondylolysis is suspected and radiographs are negative, magnetic resonance imaging, computed tomography, and/or single-photon emission computed tomography bone scintigraphy can be used for further evaluation.^4,5 In this case, the diagnosis was made based on radiographic imaging, and the patient was discharged with a scheduled follow-up with an orthopedic surgeon.

Dr Salama is a resident of radiology, resident of radiology, New York-Presbyterian Hospital/Weill Cornell Medical Center, New York. Dr Belfi is an assistant professor of radiology, Weill Cornell Medical College New York; and an assistant attending radiologist, New York-Presbyterian Hospital/Weill Cornell Medical Center, New York. Dr Hentel is an associate professor of clinical radiology, Weill Cornell Medical College, New York. He is also chief of emergency/musculoskeletal imaging and executive vice-chairman for the department of radiology, New York-Presbyterian Hospital/Weill Cornell Medical Center. He is associate editor, imaging, of the EMERGENCY MEDICINE editorial board.

A 25-year-old man with no significant past medical history presented with low-back pain that radiated down into his right thigh. The patient stated the pain began 1 week earlier when he was lifting weights and had increased in severity to the point where he was no longer able to walk or stand up straight. He had taken nonprescription nonsteroidal anti-inflammatory drugs but received no significant relief.

Radiographs of the lumbosacral spine were obtained; representative anteroposterior (AP) and lateral images are shown above (Figures 1 and 2).

The lateral view of the lumbar spine demonstrates mild anterolisthesis of L5 on S1 with the posterior cortex of L5 (white arrow, Figure 3) anterior to the posterior cortex of S1 (red arrow, Figure 3). Normally, the posterior cortices of the adjacent vertebral bodies should align. Lucency is also noted in the region of the pars interarticularis (white asterisk, Figure 3). The combination of anterolisthesis and this lucency in a young patient suggests the diagnosis of spondylolysis (pars defect).

Spondylolysis is a defect in the pars interarticularis of the vertebral arch and most commonly affects the lowest lumbar vertebrae, L5. Spondylolysis may be unilateral or bilateral. Bilateral lumbar spondylolysis can result in spondylolisthesis and instability, leading to debilitating low-back pain and neurological deficits. While the prevalence of spondylolysis is about 3% to 10% in the general population, it is more common in males than females, with a ratio of 2:1; the condition is also more prevalent in Eskimo populations (as high as 50%) and in white compared to black populations. Risk factors include a family history of spondylolysis, spina bifida occulta, and Scheuermann kyphosis.¹

The pathophysiology of spondylolysis is still uncertain. Two theories have been proposed—underlying dysplastic pars interarticularis versus repetitive microtrauma resulting in stress factors are the two proposed underlying mechanism. If patients are genetically predisposed, underlying dysplasia probably contributes to the pathology, while microtrauma triggers the actual defect.² Most patients respond well with conservative management.
When evaluating for spondylolysis, AP, lateral, 45-degree right and left oblique views, and collimated lateral views of the lumbosacral spine should be obtained. With this five-view study, up to 96.5% of pars defect can be identified.

In the general population, if spondylolysis is suspected and radiographs are negative, magnetic resonance imaging, computed tomography, and/or single-photon emission computed tomography bone scintigraphy can be used for further evaluation.^4,5 In this case, the diagnosis was made based on radiographic imaging, and the patient was discharged with a scheduled follow-up with an orthopedic surgeon.

Dr Salama is a resident of radiology, resident of radiology, New York-Presbyterian Hospital/Weill Cornell Medical Center, New York. Dr Belfi is an assistant professor of radiology, Weill Cornell Medical College New York; and an assistant attending radiologist, New York-Presbyterian Hospital/Weill Cornell Medical Center, New York. Dr Hentel is an associate professor of clinical radiology, Weill Cornell Medical College, New York. He is also chief of emergency/musculoskeletal imaging and executive vice-chairman for the department of radiology, New York-Presbyterian Hospital/Weill Cornell Medical Center. He is associate editor, imaging, of the EMERGENCY MEDICINE editorial board.