Hawai‘i Journal of Medicine & Public Health A Journal of Asia Pacific Medicine & Public Health

November 2014, Volume 73, No. 11, Supplement 2, ISSN 2165-8218

WILDERNESS MEDICINE IN HAWAI‘I AND THE PACIFIC

OUT OF THE WILDERNESS: FLIPPING THE CLASSROOM TO ADVANCE SCHOLARSHIP IN AN INTERNAL MEDICINE RESIDENCY PROGRAM 2 Dale S. Vincent MD

HIGH ALTITUDE ILLNESSES IN HAWAI‘I 4 Terry Shin MD

IS HIGH ALTITUDE PULMONARY RELEVANT TO HAWAI‘I? 7 Seth Lewis Cornell MD

PREVENTION AND TREATMENT OF FROM CAVE EXPLORATION IN HAWAI‘I 10 David W. Cowart MD; John B. Halleck BS; and Benjamin R. Park DO

THE RISKS OF : A FOCUS ON ILLNESS 13 Jennifer Hall DO

HAZARDS OF HAWAI‘I VOLCANOES NATIONAL PARK 17 Gregory M. Sprowl MD

LEPTOSPIROSIS: THE MICROSCOPIC DANGER IN PARADISE 21 William A. Londeree MD

CIGUATERA FISH IN HAWAI‘I AND THE PACIFIC 24 Nathanial K. Copeland MD; Wyatt R. Palmer DO; Paul K. Bienfang PhD

THE POTENTIAL DANGER OF EATING WILD LETTUCE: A BRIEF REVIEW OF HUMAN RAT LUNGWORM 28 Evan C. Ewers MD and Sarah K. Anisowicz MD

HEAT ILLNESS IN HAWAI‘I 33 Sarah Gordon MD

FOREIGN BODY SYNOVITIS IN THE PACIFIC 37 Caleb Anderson MD; Rodger Stitt MD; and Jefferson Roberts MD

CENTIPEDE ENVENOMATION: BRINGING THE TO HAWAI‘I AND PACIFIC ISLANDS 41 Joshua L. Fenderson MD

TROPIC : MYTH OR MENACE? 44 John McCarthy MD Out of the Wilderness: Flipping the Classroom to Advance Scholarship in an Internal Medicine Residency Program

Dale S. Vincent MD

Abstract In order to overcome barriers to participation in this project, Residents in an internal medicine residency program “flipped the classroom” we identified and leveraged several sources of motivation for in a series of learner-centered activities which included the creation of a the residents. Some residents are motivated to publish by a medical student interest group, a continuing medical education symposium, and a journal supplement focused on topics in Hawai‘i desire to be more competitive for employment and fellowship and Asia Pacific. The project encompassed both scholarly activities (discov- applications, an extrinsic source of motivation. We believed that ery, integration, application, and teaching) as well as scholarship (writing for we could also harness powerful internal motivation by having publication). The project advanced the professional formation of residents by the residents choose fun and interesting subjects with which developing competencies and producing outcomes that are key features of they were already familiar. the ACGME Next Accreditation System. Thus, the supplement became an example of a “flipped classroom.” The “flipped classroom” has been described as Introduction a “disruptive” educational model in which learners acquire This Wilderness Medicine Supplement started with a brainstorm- knowledge outside of the classroom, and consolidate that ing session with residents just before the start of the academic knowledge during mentoring that takes place inside the class- year. How do we encourage scholarly activity and also produce room.5 The characteristics of the flipped classroom have been more tangible scholarship? Indeed, the Next Accreditation Sys- succinctly summarized as: a flexible learning environment, a tem (NAS) of the Accreditation Council for Graduate Medical learner-centered culture, intentional content, and guidance from Education (ACGME) has begun to shift from emphasizing a professional educator.6 This Wilderness Medicine Supplement structure and process (scholarly activities) to outcomes (peer- exemplifies all of these characteristics. reviewed publications).1 Residents developed new skills and consolidated their learn- Here was the idea: focus on activities that the residents have ing during the supplement’s preparation. All of the papers were learned to love by living in Hawai‘i, and create a collection of written online using Google collaboration tools. Residents with scholarly reviews of common and not-so-common wilderness publishing experience mentored more junior residents. Many medicine topics for the community. Several residents had already of the authors reached out to experts in the Hawai‘i medical established a popular Wilderness Medicine Interest Group at and public health communities, anchoring their papers in lo- the University of Hawai‘i John A. School of Medicine. cal tradition and experience. They had regular meetings with The supplement would be a natural fit in the truest sense. deadlines and updates throughout the academic year, and gained Professor Ernest Boyer reimagined the range of scholarly experience with the peer review process. activities in medicine to encompass the elements of discovery, The residents also presented a six hour Wilderness Medicine integration, application, and teaching.2 By discovery, he meant Symposium with Continuing Medical Education credit. They a disciplined, methodical pursuit of new knowledge. Integration wrote learning objectives using Bloom’s , completed refers to the reworking of isolated facts to present a coherent, nondisclosure forms, and engaged in other activities that are illuminating narrative. The scholarship of application applies an integral part of the CME accreditation process. knowledge to important social and institutional problems. For many, participation in this project represented a sentinel Teaching transmits knowledge, and also transforms knowledge event in their personal professional formation. We hope you in creative and stimulating ways. Medical professional orga- sense their enthusiasm, and enjoy their papers. nizations such as the Association of Professors of Medicine have embraced this broad definition of scholarly activity.3 and Disclosures participation in scholarly activities has been an integral feature The Henry M. Jackson Foundation for the Advancement of of residency training. Military Medicine, Inc. provided financial support for this The ACGME has recently begun to ask residencies to report supplement. Dr. Vincent reported no conflicts of interest. the outcomes of scholarship in residency programs.1 By scholar- ship, the ACGME means the creation of published works in the Disclaimer peer-reviewed medical literature. Internal medicine and other The views expressed in this abstract/manuscript are those of primary care residents already have grueling schedules and a the author and do not reflect the official policy or position of daunting body of knowledge to master during their short, three- the Department of the Army, Department of Defense, or the year residencies, so this new expectation represents a special US Government. challenge.4

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 2 Author’s Affiliation: References Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 1. Philibert I, Leih-Lai M, Miller R, Potts JR, Brigham T, Nasca TJ. Scholarly activity in the Next Accreditation System: moving from structure and process to outcomes. J Grad Med Educ. Correspondence to: 2013;5(4):714. 2. Boyer EL. Scholarship reconsidered: priorities of the professoriate. The Carnegie Foundation Dale S. Vincent MD; Program Director; Internal Medicine Residency Program for the Advancement of Teaching. San Francisco: Jossey-Bass, 1990. Tripler Army Medical Center, Honolulu, HI 96859; 3. Gerachi SA, Hollander H, Babbott SF, Buranosky R, Devine DR, Kovach RA, Berkowitz. AAIM Ph: (808) 433-6793; Email: [email protected] report on master teachers and clinician educators part 4: faculty role and scholarship. Am J Med. 2010 (November);123(11):1065-1069. 4. Ledford CJW, Seehusen DA, Villagran MM, Cafferty LA, Childress MA. Resident scholarship expectations and experiences: sources of uncertainty as barriers to success. J Grad Med Educ. 2013;5(4):564. 5. Mehta NB, Hull AL, Young JB, Stoller JK. Just imagine: new paradigms for medical education. Acad Med. 2013;88(10):1418-1423. 6. Kharbach, M.The four pillars of flipped learning. Educational Technology and Mobile Learning. Found at http://www.educatorstechnology.com/2014/05/the-four-pillars-of-flipped-learning.html. Accessed June 5, 2014.

Wilderness Medicine in Hawai‘i and the Pacific

Guest Editors

Seth L. Cornell MD William A. Londeree MD Gregory M. Sprowl MD Dale S. Vincent MD

Nu‘uanu from Pali Notches (Photo: William Harner MD)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 3 High Altitude Illnesses in Hawai‘i

Terry Shin MD

Abstract increased blood flow.5 Recent research, suggests that the tight- High Altitude (HAH), Acute Mountain Sickness (AMS), and High fit hypothesis is an oversimplification of complex underlying Altitude (HACE) are all high altitude related illnesses in order of severity from the mildly symptomatic to the potentially life-threatening. High processes. theory describes a complicated networking altitude illnesses occur when travelers ascend to high altitudes too rapidly, of hypoxic ventilator response, vessel permeability, multiple which does not allow enough time for the body to adjust. Slow graded ascent chemical mediators, and sodium/potassium ATPase failure.5 to the desired altitude and termination of ascent if AMS symptoms present are AMS symptoms can occur as early as an hour after ascent, but keys to illness prevention. Early recognition and rapid intervention of AMS can typically occur 6 to 10 hours following ascent to higher alti- halt progression to HACE. Pharmacologic prophylaxis with acetazolamide is a tudes.6 There are no known diagnostic modalities that reliably proven method of prevention and treatment of high altitude illness. If preven- confirm the diagnosis of AMS. AMS is a clinical diagnosis tion fails then treatment modalities include supplemental , supportive therapy, hyperbaric treatment, and dexamethasone. Given the multitude of based on history and symptoms. At the and Mountain visitors to the mountains of Hawai‘i, high altitude illness will continue to persist Medicine Symposium in Lake Louise, Canada a consensus as a prevalent local condition. This paper will emphasize the prevention and was established for the diagnosis. This group defined AMS as early diagnosis of AMS so that the illness does not progress to HACE. an unacclimatized person who recently ascended an altitude above 2500 m who presents with headache, plus the presence Relevance to Hawai‘i and Asia Pacific of at least one of the following conditions: gastrointestinal High altitude illnesses typically occur with ascent above 2,500 symptoms (, , ), /weakness, m (8,202 ft) but can occur at altitudes as low as 2000 m (6,562 /lightheadedness, or difficulty with sleep.7 A scoring ft).1 There are three mountain peaks on the Hawai‘i islands that table was created to diagnose and predict the severity of AMS. exceed this height threshold. Mauna Kea, the largest mountain (Table 1) The Lake Louise Scoring System Table includes a on the island of Hawai‘i rises to 4205 m (13,796 ft) from sea total of 5 questions. Any individual with a self reported score level. Mauna Loa, also on the island of Hawai‘i, peaks at 4,169 of at least 3 or more is considered to have AMS. A score of 3-5 m (13,679 ft).2 Haleakala, the third highest mountain, is on the is considered mild AMS and a score of 6 or more is considered island of Maui and rises to 3,055 m (10,023 ft).3 Both tourists and to be moderate to severe. island residents are permitted to travel via a motorized vehicle to the peaks of these mountains. AMS is a common presentation Table 1. Lake Louise Score for AMS in individuals who reach the summit of these mountains due to Self Reported Score Severity Score rapid changes in altitude. One survey of visitors to Mauna Kea Headache No headache 0 found that 30 percent of tourists and 69 percent of astronomy Mild headache 1 staff developed symptoms consistent with AMS.4 Moderate headache 2 Severe headache, incapacitating 3 Clinical Description Gastrointestinal Symptoms None 0 Poor appetite or nausea 1 The most common and initial presentation in high-altitude illness Moderate nausea&/or vomiting 2 is a headache. This headache is described as high altitude head- Severe nausea &/or vomiting 3 ache (HAH) and will occur in approximately 80% of individuals Fatigue/Weakness Not tired or weak 0 that ascend to altitude.5 HAH can present as a generalized tension Mild fatigue/weakness 1 or migraine headache. AMS is thought to be the progression Moderate fatigue/weakness 2 Severe fatigue/weakness 3 of HAH where the headache persists with additional systemic Dizziness/Lightheadedness Not dizzy 0 symptoms. At the opposite of the end of the illness spectrum Mild dizziness 1 from HAH is the potentially lethal condition known as high Moderate dizziness 2 altitude cerebral edema (HACE). HACE is considered the end Severe dizziness, incapacitating 3 stage of neurologic high . Early recognition of Difficulty Sleeping Slept as well as usual 0 AMS can provide an opportunity for intervention and treatment Did not sleep as well as usual 1 Woke many times, poor sleep 2 so that the condition does not progress to HACE. Could not sleep at all 3 The exact mechanisms of high altitude illness are still un- TOTAL SCORE clear. For the last 20 years, the “tight-fit hypothesis” was the predominant explanation. The tight-fit hypothesis suggests that Self Reported Score inadequate cerebral spinal fluid buffer places individuals at risk AMS score >= 3 MILD AMS for increased intracranial from edema formation and AMS score >= 6 MODERATE /SEVERE AMS

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 4 Other diagnoses should be pursued if symptoms persist Pharmacologic prophylaxis with is an option that greater than three days, there is a lack of response after descent, can be utilized to limit the effects of altitude sickness. Acet- or there is an absence of a headache. A azolamide, a carbonic anhydrase inhibitor, is the drug of choice for AMS includes , migraine, , CNS for prevention of AMS. Multiple trials have demonstrated the infection, transient ischemic attack, exposure effectiveness of acetazolamide for AMS prevention and it is and substance abuse.8 currently a Grade 1A recommendation per the Wilderness High altitude cerebral edema is a rare condition which is Medical Society.14 Acetazolamide is indicated for rapid ascent considered the end stage of high altitude illnesses. HACE is rare to altitudes greater than 3000 m (9843 feet).15 Prophylaxis with and the incidence is roughly seen in only 1% to 2% of people acetazolamide would be most applicable to individuals travel- ascending to heights greater than 4500 m (14,763 ft).9 HACE, ing to Mauna Kea and Mauna Loa who plan prolonged stays at however, can occur at elevations as low as 2750 m (9022 ft).6 high altitudes. Other indications for prophylaxis include rapid HACE can be visualized with MRI, which presents as reversible gain in sleeping altitude in a day and a history of AMS. The white matter edema within the corpus callosum and splenium.10 common dose regimen for acetazolamide ranges from 125 mg The two primary clinical presentations of HACE are altered to 250 mg twice a day.5 consciousness and . The condition can progress rapidly If an individual develops AMS, the treatment should include from and irrational behavior to lethargy and halting ascension and awaiting acclimatization. A clear indica- . will typically occur as a result of brain herniation. tion for immediate descent is a severe neurologic change. The Physical exam findings include truncal ataxia, papilledema, existence of only a few reported incidents in Hawai‘i of serious retinal hemorrhage, and other focal neurologic deficits. Due to altitude illness might be explained by the ability to descend its lethality, patients presenting with any such symptoms should rapidly from the mountains such as on Mauna Kea, leading to be treated as if diagnosed with HACE until proven otherwise. prompt reversal of any adverse effects.5 Lightweight portable hyperbaric chambers commonly known Example Case as Gamow bags can be used when immediate descent is not A male Kailua resident drove up to the top of the volcano, possible. They consist of lightweight fabrics that serve as a pres- Mauna Loa. At approximately 11,000 feet, he hiked along a sure bag with manual air pumps to create a hyperbaric chamber. trail up to his destination of 13,200 feet.11 During his ascent, he Prospective studies have demonstrated hyperbaric chambers are began to develop headache, nausea, and lightheadedness that effective for immediate relief of AMS and HACE.16 They are eventually progressed to bouts of persistent emesis. Despite usually limited to mountaineering expeditions and are typically oral fluid hydration and attempting to stay warm, his symp- not utilized in lower altitudes. toms persisted. He was eventually air lifted from his location and was subsequently transferred to Hilo Medical Center. He Treatment in Non-Austere Environments was discovered to have lost 10 pounds in a 24-hour period. He After halting ascent any unnecessary physical exertion should was administered intravenous fluids and prescribed be kept to a minimum. Treatment typically involves supportive for his headache. He reportedly recovered without care and initiation of low-flow supplemental oxygen to maintain significant sequelae. arterial oxygen saturation to greater than 90%. Even though in other geographic locations oxygen tanks are typically carried Treatment in Resource Constrained by climbers on ascents that involve high altitudes, in Hawai‘i, Environments supplemental oxygen will most likely be available only to Prevention is the cornerstone to averting high-altitude illnesses, EMS or in hospital settings. Supplemental oxygen should be especially when ascending mountains of high altitude. One of administered in the inpatient setting for approximately 1 to 2 the simplest and safest ways of preventing AMS is by ascend- days or until AMS symptoms resolve.6 Patients often present ing to higher altitudes slowly along graded elevations. Two dehydrated and should receive oral or intravenous hydration such methods are staged ascent and graded ascent. In staged as appropriate. They can also be treated with Acetazolamide, ascent, an individual will ascend at an average pace to a mod- but it should be administered as early as possible to capture erate altitude and remain there for three or more days to allow any benefit. Symptomatic therapy typically includes acclimatization before further ascension. Graded ascent limits such as NSAIDs or acetaminophen for . Antiemetics the gain in altitude with partial acclimatization throughout the should be provided to treat nausea and vomiting. Treatment ascent.12 For prolonged habitation at altitudes above 3000 m, with dexamethasone can also relieve symptoms but it is usually it is recommended that individuals limit sleeping altitude to no limited to emergency cases where progression to HACE is prob- more than 300 meters above the previous sleeping altitude.13 able. The usual dosage is 4 mg every 6 hours until resolution of A combination of the two methods is considered optimal in symptoms.6 A stationary hyperbaric chamber is an additional preventing high altitude illness. Graded ascent would be the treatment option but is not required unless there is a concern most practical method in high-altitude illness prevention given for refractory HACE. the ability to rapidly obtain high altitudes in Hawai‘i.

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 5 Conclusion Correspondence to: Terry Shin MD; 1 Jarrett White Rd, Honolulu, HI 96859; High Altitude Illness is recognized as a notable concern in high Email: [email protected] altitude medicine, and public awareness is vital for prevention. Education of healthcare providers to readily recognize and References appropriately treat individuals presenting with symptoms is 1. Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society Consensus Guidelines for the Prevention and Treatment of Acute Altitude Illness. Wilderness Environ Med. 2010; crucial to preventing fatalities. Acute Mountain Sickness does 21:146. occur on the islands of Hawai‘i, but the progression of AMS to 2. U.S. Geological Survey (USGS) [Internet]. [updated 23 Jun 2013; cited 03 Dec 2013]. Available from: http://hvo.wr.usgs.gov/volcanoes/maunakea/ HACE is uncommon given the local topography which allows 3. U.S. Geological Survey (USGS) [Internet]. [updated 23 Jun 2013; cited 03 Dec 2013]. Available for quick descent to lower altitudes. Nevertheless, the case pre- from: http://hvo.wr.usgs.gov/volcanoes/haleakala/. 4. Onopa J, Haley A, Yeow ME. Survey of acute mountain sickness on Mauna Kea. High Alt Med sented in this article illustrates the susceptibility of climbers to Bio. 2007 Fall;8(3):200-5. AMS with the potential progression to HACE in Hawai‘i. The 5. Wilson MH, Newman S, Imray CH. The cerebral effects of ascent to high altitudes. Lancet Neurol. 2009;8:175-91. key to preventing high altitude illnesses ultimately relies on an 6. Gallagher SA, Hackett PH. High-altitude illness. Emerg Med Clin North Am. 2004;22:329. established system to properly educate travelers and residents 7. Roach RC, Bartsch P, Oelz O, Hackett P. Lake Louise AMS Scoring Consensus Committee. The Lake Louise acute mountain sickness scoring system. In: Hypoxia and Molecular Medicine. who visit the mountains of Hawai‘i. Burlington: Charles S Houston, 1993:272-274. 8. Hackett PH, Roach RC. High-altitude illness. N Engl J Med. 2001;345:107. 9. West JB, American College of Physicians, American Physiological Society. The physiologic Disclosures basis of high-altitude diseases. Ann Intern Med 2004; 141:789. The author reported no conflicts of interest. 10. BA, Wright AD, Wilson MH, et al. High altitude ataxia—its assessment and relevance. Wilderness Environ Med. 2011; 22:172. 11. Bernardo, Rosmarie, editor. Mauna Loa’s high. Honolulu Star-Bulletin. (updated 08 Apr 2002; Disclaimer cited 03 Dec 2013). 12. Mountain Operations, Field Manual 3-97.6 (90-6), Headquarters, Department of the Army. 28 The views expressed in this paper are those of the author and November 2000. do not reflect the official policy or position of the Department 13. Milledge JS. Acute Mountain Sickness. . 1983; 28: 641-645 14. Luks AM, McIntosh SE, Grissom CK, Auerbach PS, Rodway GW, Schoene RB, Zafren K, of the Army, Department of Defense or the U.S. Government. Hackett PH; Wilderness Medical Society. Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness. Wilderness Environ Med. 2010 Author’s Affiliation: Jun;21(2):146-55. 15. Low EV, Avery AJ, Gupta V, Schedlbauer A, Grocott MP. Identifying the lowest effective dose Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 of acetazolamide for the prophylaxis of acute mountain sickness: systematic review and meta- analysis. BMJ. 2012;345:e6779. 16. Kasic JF, Yaron M, Nicholas RA, Lickteig JA, Roach R. Treatment of acute mountain sickness: Hy- perbaric versus , Annals of . 1991 October;20(10):1109-1112.

Mauna Kea Road (Photo: Jacob M. Mathew DO)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 6 Is High Altitude Relevant to Hawai‘i?

Seth Lewis Cornell MD

Abstract pedition, the patient noted dyspnea, weakness, and cough that High altitude clinical syndromes have been described in the medical literature subsequently worsened over the fourth day. The patient was but may be under recognized in the state of Hawai‘i. As tourism increases, high transported to the nearest hospital where he was found to have altitude injuries may follow given the easy access to high altitude attractions. Visitors and clinicians should be aware of the dangers associated with the a of 99.6F, a of 120/80, a of rapid ascent to high altitudes in the perceived comfort of a vehicle. This paper 96 and respirations of 30. His physical exam was remarkable will review the basic pathophysiology, prevention, and treatment of the most for moderate , with bilateral coarse pulmonary rales serious of the high altitude clinical syndromes, high altitude pulmonary edema. noted on auscultation. There was no cardiomegaly, peripheral edema, or jugular venous distention. The patient had a leuko- Introduction cytosis of 13,000 and a chest radiograph that revealed bilateral The physiologic effects of high altitude are complex and not pulmonary edema. The patient experienced rapid resolution simply limited to hypoxia.1 This is reflected by the varying of his symptoms within 36 hours of admission. On further ability of individuals to acclimate to changes in altitude. High questioning, the patient described similar symptoms during a altitude clinical syndromes are diverse and can range from life previous mountain expedition three years earlier with complete threatening high altitude cerebral and pulmonary edema to less resolution of his dyspnea after descent from altitude. severe acute mountain sickness.2 The rate of ascent is often directly related to the severity of the clinical syndrome.3 High Discussion altitude pulmonary edema (HAPE) is the most frequent cause Hypoxia is the primary insult of high altitude exposure.9 Baro- 4 of altitude related fatalities. Although the pathophysiology is metric pressure and the of inspired oxygen (PIO2) not completely understood, HAPE is easily treatable; unrec- decreases in a logarithmic manner as altitude is increased.10 At 5 ognized, it may be fatal. altitudes below 10,000 feet, the changes in PIO2 and resultant

partial pressure of arterial oxygen (PaO2) routinely have little

Relevance to Hawai‘i and Pacific Region effect on the arterial oxygen saturation (SaO2). However, above

Mauna Kea is the highest point in the Pacific Basin and if 10,000 feet small decreases in PaO2 can have significant effects measured from base to summit, the tallest mountain in the on SaO2.11 Fortunately, the human body has innate physiologic world. From its origins deep within the Pacific Ocean, to its mechanisms that allow for altitude acclimatization. high altitude peak, this dormant volcano rises approximately The process of acclimatization is complex and its success 32,000 feet and stands at 13,796 feet above sea level. This sa- varies from individual to individual.12 The rate of altitude gain cred mountain, once regarded as “the abode of gods,” is now directly correlates with the severity of high altitude pathology and visited by several hundred visitors daily, usually by vehicle. therefore it is recommended that altitude gains be incremental, Poli‘ahu, the ancient snow goddess of Mauna Kea and rival of allowing time for physiologic adjustment. The recommended Pele, now keeps watch over the world’s largest collection of rate of ascent and time allowed for acclimatization is dynamic observatories, which occupy the summit of the hallowed peak.6 and based on an individual’s overall risk for developing a high The Hawaiian Islands offer lowlanders the rare opportunity altitude illness. of ascending from near sea level to elevations in excess of is an early response to low PaO2 and works two and a half miles. In fact, many of these volcanic peaks to enhance oxygen delivery to tissues. Hyperventilation causes are readily accessible by automobile, allowing people of all a respiratory alkalosis which triggers renal excretion of bicar- backgrounds to rapidly visit areas previously limited to the bonate as a compensatory mechanism to normalize serum pH. determined mountaineer. Although easy access affords many Maximum ventilation with renal adjustment is typically reached the opportunity to experience the wonders of the volcanic god- within one week at a given altitude. The degree of an individual’s dess, Pele, it also exposes many tourists to the adverse effects hyperventilatory response may correlate with overall acclima- of high altitude physiology.7 tization success and the prevention of high altitude illness. Renal secretion of erythropoietin also occurs in response to Case Report from the Medical Literature hypoxia. Increased proliferation of red blood cells begins within One of the first reported cases of high altitude pulmonary four days, however, the complete effects of erythropoiesis may edema appeared in a 1960 article by Dr. Charles S. Houston.8 take several weeks. The success of acclimatization does not Dr. Houston described a healthy 21 year old male who made a seem to correlate with the degree of erythropoiesis. Changes in cross country ski trip from Aspen, Colorado (elevation 7,890ft) mitochondrial architecture and quantity have also been proposed over a 12,000 foot mountain pass. On the third day of the ex- as another mechanism of altitude acclimatization.13

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 7 When acclimatization to altitude does not occur, several high- worsen the pulmonary edema. If attempts at re-ascent are made, altitude syndromes may happen. The high-altitude syndromes additional time should be allowed for proper acclimatization. (acute mountain sickness, high altitude cerebral edema, and high altitude pulmonary edema) likely represent a spectrum of Treatment in Non-Austere Environments pathophysiology. Symptoms often overlap making an accurate As most cases of HAPE resolve with descent from altitude, clinical distinction difficult. additional treatment is not typically required, however, severe HAPE is the leading cause of death related to high altitude cases of HAPE may require hospitalization with more intensive syndromes. Symptom onset is often encountered within 2-4 days medical care. In addition to descending from altitude, supple- of arrival at high altitude (approximately 10,000 ft), however, mental oxygen is a mainstay of therapy. Hypoxia frequently incidents have occurred sooner and at lower altitudes. Affected resolves with low flow oxygen, though more severe cases may individuals typically complain of , cough, dyspnea, and require high flow or even continuous positive airway pressure fatigue. Physical examination may reveal a cyanotic appearance (CPAP). Portable hyperbaric chambers have also been used with demonstrating and , along for HAPE treatment. Endotracheal intubation with mechani- with a possible . Predicting which individuals will be most cal ventilation is infrequently required but may be necessary. susceptible to HAPE is difficult, though previous episodes seem There are several proposed medications often used in the to be the strongest predictor of future susceptibility. Certain adjunctive treatment of HAPE. , a dihydropyridine underlying medical conditions such as lung disease, heart , is the most well studied of the treatment disease, diabetes, and pregnancy, may also put individuals at modalities and works through which acts to lower increased risk of developing HAPE.14-17 PAP. Likewise, phosphodiesterase inhibitors such as sildenafil The pathophysiology of HAPE is not completely understood, may blunt the hypoxic pulmonary response, although increased pulmonary arterial pressure (PAP) seems to thus improving PAP. Other previously used adjuncts include be uniformly present. Pulmonary vasoconstriction and resultant diuretics, corticosteroids, carbonic anhydrase inhibitors, and increased PAP is a known response to hypoxia. However, in- inhaled beta-agonists, though current guidelines do not support creased PAP alone cannot explain HAPE, as hypoxia and PAP their routine use in the treatment of HAPE.20 are common findings among asymptomatic mountaineers at altitude.18 Increased capillary permeability, perhaps secondary Conclusion to increased capillary stress from PAP, has been proposed as a High altitude pulmonary edema is an easily treatable, though possible mechanism in HAPE.19 potentially fatal, syndrome of the acute mountain illnesses. With education and implementation of proper preventive techniques, Treatment in Resource-Constrained such as a judicious rate of ascent above 10,000ft and nifedipine Environment when indicated, HAPE can often be avoided. Several of the Simple awareness and education of HAPE often allows for volcanic peaks found among the Hawaiian Islands rise well appropriate preventive techniques to be used. All individuals above 10,000ft and many are directly accessible by vehicle should be encouraged to slow their rate of ascent once above and overly rapid ascent. Proper education and recognition of 8,500 ft. For prolonged expeditions, most experts recommend HAPE is paramount in decreasing its incidence and reducing no greater than an increase of 1,500 ft per day for sleeping its morbidity. elevations, with no elevation gain every third or fourth day. For individuals with a prior history of HAPE, pharmacologic Disclosures prophylaxis should be considered. Numerous pharmacologic The author reported no conflicts of interest. agents have been used to prevent HAPE (nifedipine, salmeterol, tadalafil, dexamethasone, acetazolamide), however, current Disclaimer guidelines only recommend the use of nifedipine.20 Most ex- The views expressed in this manuscript are those of the author perts recommend 30 mg of sustained release nifedipine every and do not reflect the official policy or position of the Department 12 hours which should be started on the day prior to ascent and of the Army, Department of Defense, or the US Government. continued until descent is initiated. Prompt recognition of HAPE is essential, as most cases Author’s Affiliation: Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 improve dramatically with descent from altitude. Emergent cases require rapid descent, whereas less severe symptoms Correspondence to: may improve with a moderate decrease of 1,500ft to 3,000ft. Seth Cornell MD; 1 Jarrett White Rd, Honolulu, HI 96859; Email: [email protected] Since patients frequently suffer from hypoxemia during HAPE, exertion during the descent should be minimized as much as pos- sible and supplemental oxygen administered. Euthermia should also be maintained to lessen any increases in PAP, which may

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 8 References 11. Sutton J, Reeves J, Wagner P, et al. Operation Everest II: Oxygen transport during 1. Hackett P, Roach R. High-altitude medicine and physiology. In: Auerbach P. Wilderness Medicine. at extreme simulated altitude. J Appl Physiol. 1985;64:1309-21. 6th ed. Philadelphia, PA: Elsevier Mosby; 2012:2-33. 12. Mortimer H, Patel S, Peacock A. The genetic basis of high-altitude pulmonary oedema. Phar- 2. Bartsch P, Swenson E. Acute high-altitude illnesses. N Engl J Med. 2013;368:2294-302. macol Ther. 2004;101:183-92. 3. Schoene R. Illnesses at high altitude. Chest. 2008;134:402-416. 13. Chitra L, Boopathy R. Adaptability to hypobaric hypoxia is facilitated through mitochondrial 4. Hall D, Duncan K, Baillie J. High altitude pulmonary oedema. J R Army Med Corps. 2011;157:68- bioenergetics: an in vivo study. Br J Pharmacol. 2013;169:1035-47. 72. 14. Luks A, Swenson E. Travel to high altitude with pre-existing lung disease. Eur Respir J. 5. Luks A. Do we have a “best practice” for treating high altitude pulmonary edema? High Alt Med 2007;29:770-92. Biol. 2008;9:111-4. 15. Bartsch P, Gibbs J. Effect of altitude on the heart and lungs. Circulation. 2007;116:2191-202 6. Maly K, Maly O. Executive Summary. In: Mauna Kea – Ka Piko Kaulana O Ka ‘Aina. A collection 16. Brubaker P. Adventure travel and type 1 diabetes: the complicating effects of high altitude. of native traditions, historical accounts, and oral history interviews for: Mauna Kea, the lands Diabetes Care. 2005;28:2563-72. of Ka‘ohe, Humu‘ula and the “‘Aina Mauna on the island of Hawai‘i. KPA Study. Hilo, HI: Kumu 17. Jean D, Leal C, Kriemler S, Meijer H, Moore L. Medical recommendations for women going to Pono Associates; 2005:5-8. altitude. High Alt Med Biol. 2005;6:22-31. 7. Onopa J, Haley A, Yeow M. Survey of acute mountain sickness on Mauna Kea. High Alt Med 18. Maggiorini M, Melot C, Pierre S, et al. High-altitude pulmonary edema is initially caused by an Biol. 2007;8:200-5. increase in capillary pressure. Circulation. 2001;103:2078-83. 8. Houston C. Acute pulmonary edema of high altitude. N Engl J Med. 1960;263:478-80. 19. Swenson E, Maggiorini M, Mongovin S, et al. Pathogenesis of high-altitude pulmonary edema: 9. Hackett P, Roach R. High-altitude illness. N Engl J Med. 2001;345:107-14 inflammation is not an etiologic factor.JAMA . 2002;287:2228-35. 10. West J. The physiologic basis of high-altitude diseases. Ann Intern Med. 2004;141:789-800. 20. Luks A, McIntosh S, Grissom C, et al. Wilderness medical society consensus guidelines for the prevention and treatment of acute altitude illness. Wilderness Environ Med. 2010;21:146-55.

Mauna Kea Summit at Sunset (Photo: Jacob M. Mathew DO)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 9 Prevention and Treatment of Injuries from Cave Exploration in Hawai‘i

David W. Cowart MD; John B. Halleck BS; and Benjamin R. Park DO

Abstract the patient at 1720. It then took 10.5 hours to get the patient to Cave exploration is a popular activity in the that can be chal- the surface using a drag stretcher, requiring periodic off loading lenging, thrilling, and dangerous. In addition to common risks associated with caves on the mainland, caves in Hawai‘i may be filled with tidal water, from the stretcher to maneuver crawl spaces and obstacles. He or contain large pools of water that are accessible only through underwater reached the surface at 0550 the next morning and was admitted entrances. This paper will discuss common injuries in caves on the mainland to the hospital at 0815. This case highlights the prolonged time United States, as well as cave related injuries in Hawai‘i as reported to the that may be required to extract an injured person from a cave. National Speleological Society from 1984-2013. Treatment in Austere Environment Introduction Treatment can be broadly classified as self-aid, rescuer treat- Cave exploration is a popular activity among well-trained cavers ment, and definitive hospital care. Training and preparedness as well as untrained members of the general population. Over are both extremely important preventative measures which two million people visit thousands of caves in the United States significantly decrease the risk and severity of .2 The each year.1, 4 Caves are often , dark, and contain confusing most common reported incidents in Hawai‘i are falls (41.7%), tunnels with tight and twisting spaces. An unfamiliar environ- (30.6%), and being lost or stranded (8.3%) (Table 1). ment has inherent dangers, and injuries can be serious, especially A national survey suggested that experienced cavers are much in the inexperienced cave explorer. less likely to sustain serious injuries and are more likely to take preventative measures, such as appropriate clothing to prevent Relevance to Hawai‘i and also wearing of helmets.2 The Hawaiian islands are home to numerous caves, many formed Self-aid is the initial treatment strategy immediately following by lava tubes during the islands’ development. Hawai‘i attracts an injury. Since most injuries occur to inexperienced millions of tourists annually and this brings increased risks and cavers, resources (ie, water, batteries, heat source, tourniquet, dangers to visitors who explore them and are unfamiliar with compression bandages) are likely to be limited. Falls, the most their challenges. From 1980 through 2008, 877 nationwide common type of reported injury in Hawai‘i, can result in multiple incident reports were sent to the National Speleological Society injuries, usually involving sprains or fractures but also head (NSS) Accident Reports, involving 1356 individual cavers, and trauma. Injured cavers need to be resourceful during this initial eighty one (6%) had fatal outcomes. From 1984 through 2013, phase of treatment. One Hawai‘i incident reported to the NSS a total of 33 incidents involving 35 people were reported from described a photographer who fell and fractured his leg while Hawai‘i, and 18 (51.4%) died as a result of injuries sustained at the entrance of a cave. He used clothing to brace his leg with during cave exploration. and medical management the camera tripod, enabling him to walk a sufficient distance to are clearly pertinent topics for Hawai‘i in view of these serious seek help. The majority of cases that result in successful rescue injuries and outcomes. are typically non-life threatening injuries. Stabilization of a sprain or fracture with a simple improvised Illustrative Case brace or splint is often sufficient until further medical care is Caves often present rough terrain and tight passageways, and available. If immediate, life-threatening concerns (bleeding may allow for passage of only one individual at a time. This or hemorrhage) are present, compression should be applied may prolong the time to reach an injured patient, and to man- continuously during the rescue. Use of improvised tourniquets age an extraction. Primary interventions such as securing an is controversial but may provide life-saving control of hemor- airway and monitoring for and circulation are more rhage at the expense of a limb in prolonged extractions.5 A list difficult. For example, if a patient vomits during transport of useful items in a rescue kit is shown in Table 3. through a tight passageway, keeping the airway clear may be Although the Hawaiian climate is tropical, hypothermia is challenging. One case report describes an incident that took a real threat in a cave, which may be significantly cooler and place in Yorkshire in which an individual became trapped and wetter than the surface. Injured cavers should attempt to re- pinned by a dislodged boulder while crawling through a cave.3 main dry and rescuers should remove any wet clothing, wrap The patient, with two friends, had entered the cave at 1000 and the patient in waterproof garments and warm with blankets or after 2 hours was approximately one-half mile from the cave body contact whenever possible during prolonged extractions.5 entrance. It took his friends one hour and forty five minutes to The injured caver can also be given warm fluids by mouth, as reach the surface and call for help. The rescue team, including injuries allow, helping to increase the core body temperature. a physician, arrived on site at 1630 and reached and released

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 10 Table 1. Mechanism of Incident (Data from NCRC Incident Reports) Number Incident Fatality (%) Injury and aid (%) Injury without aid (%) Aid only, no injury (%) (% of total # incidents) Caver Fall 15 (41.7) 3 (21.4) 8 (50) 3 (21.4) 1 (7.1) Drowning 11 (30.6) 11 (100) 0 (0) 0 (0) 0 (0) Lost or Stranded 3 (8.3) 0 (0) 0 (0) 3 (100) 0 (0) Near Drowning 2 (5.6) 0 (0) 2 (100) 0 (0) 0 (0) Fell and Drown 1 (2.8) 1 (100) 0 (0) 0 (0) 0 (0) Laceration 1 (2.8) 0 (0) 1 (100) 0 (0) 0 (0) 1 (2.8) 1 (100) 0 (0) 0 (0) 0 (0) Unknown 1 (2.8) 1 (100) 0 (0) 0 (0) 0 (0) Found Murdered Victim 1 (2.8) 1 (100) 0 (0) 0 (0) 0 (0) 36 18 10 6 1

Table 2. Months of Reported Incidents (Data from NCRC Incident Table 3. Suggested items of a Cave Medic Kit5 Reports) Contents of a Basic Cave Medic Kit Additions for Personnel with Higher Month of Year Number (%) Level of Training/Licensing January 3 ● Scissors ● Narcotic/pain medications ● Adjustable Cervical Collar ● Intramuscular February 6 ● Duct Tape ● Injectable 1% lidocaine syringes and March 2 ● Gauze bandages needles for regional nerve blocks ● Flexible splints ● Povidone-iodine prep pads April 2 ● Elastic wrap ● Scalpel blades ● Personal Protective Equipment May 2 ● Stethoscope June 1 ● Blood pressure cuff ● Pencil with waterproof paper July 5 ● Digital August 1 ● Safety pins ● Nasal and oral airways September 3 October 1 November 5 Disclosures December 2 The authors reported no conflicts of interest. Winter 1 Spring 1 Disclaimer Unknown 1 The views expressed in this manuscript are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the US Government. Conclusion The type of injuries sustained in caves can vary greatly and, in Acknowledgements The National Speleological Society (NSS) for allowing access to their incident many cases, inexperienced cavers are underprepared for injuries reports and to John Halleck for his personal experience, authorship and and rescuers have limited medical training. Bleeding should guidance on this project. be controlled, fractures and sprains stabilized, and the injured patient kept warm, dry, and hydrated. Cervical spine stabiliza- Authors’ Affiliation: tion should be considered in any patient that has sustained a Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 fall. Most people with life-threatening caving injuries do not Correspondence to: survive due to prolonged time to definitive care. Therefore, David W. Cowart MD; 1 Jarrett White Rd, Honolulu, HI 96859; life-threatening injuries such as heavy bleeding, hypothermia, Email: [email protected] crush injuries, and respiratory distress must be recognized and treated to avoid progression to fatal outcomes. Many patients will be cold, scared and experience attacks. Rescuers should be prepared to reassure these individuals as much as possible.

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 11 References Additional Public Resources 1. Stella-watts AC, Holstege CP, Lee JK, Charlton NP. The epidemiology of caving injuries in the National Cave Rescue Commission: www.caves.org/commission/ncrc/national. United States. Wilderness Environ Med. 2012;23(3):215-22. National Speleological Society (NSS) Accident Reports: http://www.caves.org/pub/aca/13index.html. 2. Ashford DA, Knutson RS, Sacks JJ. Injury among cavers: results of a preliminary national survey. J Sports Med Phys Fitness. 1999;39(1):71-3. 3. Craven SA. Some medical aspects of caving accidents: illustrated by a case history. Injury. 1973;5(2):94-9. 4. Krau SD. Summer activities: incidents and accidents. Crit Care Nurs Clin North Am. 2013;25(2):287-95. 5. Hudson S, McCurley L, Mortimer R. Wilderness Medicine: Caving and Cave Rescue. 6th ed. Philadelphia, PA: Elsevier Inc, 2012.

Cave Waterfall (Photo: Jacob M. Mathew DO)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 12 The Risks of Scuba Diving: A Focus on

Jennifer Hall DO

Abstract Decompression Illness includes both (DCS) and cific class of diving (ie, recreational, commercial, military, or 3,4 Pulmonary Overinflation Syndrome (POIS), subsets of diving-related injury scientific). Assuming an average of fifteen diving-related related to scuba diving. DCS is a condition in which gas bubbles that form injuries per 10,000 dives, and approximately 200 daily dives while diving do not have adequate time to be resorbed or “off-gassed,” result- across the Hawaiian Islands, we would predict one DCS or ing in entrapment in specific regions of the body. POIS is due to an overly POIS event every week.3,4 rapid ascent to the surface resulting in the rupture of alveoli and subsequent extravasation of air bubbles into tissue planes or even the cerebral circulation. Example Cases Divers must always be cognizant of dive time and depth, and be trained in the management of decompression. A slow and controlled ascent, plus proper Case 1 control of can reduce the dangerous consequences of pulmonary A 28-year-old US Navy SEAL performed a working dive using . The incidence of adverse effects can be diminished with safe scuba to secure an apparatus on the bottom to buoy lines at the practices, allowing for the full enjoyment of this adventurous aquatic sport. water surface. This entailed multiple descents and ascents. The seas had been choppy with swells of two to four feet and cur- Introduction rents at roughly one to two knots, thus creating a challenging Scuba diving is a sport with exhilaration, beauty, and fasci- environment. descended to 60 feet and ascended to nation; however, the risks involved are often not advertised. the surface, intermittently holding his breath while bobbing up Two specific conditions can turn a fantastic dive into trouble, and down on the surface. After obtaining the next piece of work with occasional fatal outcomes: Decompression Sickness and equipment from the zodiac boat, he made another descent to 60 Pulmonary Overinflation Syndrome. After spending six years ft, followed by ascent to the surface. This time, he noted blurry as a US Navy Diving Medical Officer, I will share some case vision in his right eye, thinking he had merely gotten seawater reports and discuss the physiology, clinical presentation, and under his mask. The diver proceeded to the bottom again to treatments for these diving-related injuries. finish his job. Upon ascent, he experienced mild to Decompression Illness includes both Decompression Sick- the right side of his face. The diver was brought into the zodiac ness (DCS) and Pulmonary Overinflation Syndrome (POIS), boat and described his symptoms to the . His subsets of diving-related injury related to scuba diving. Divers symptoms quickly progressed to involve numbness and tingling should understand their limitations and how to prevent adverse in his left upper extremity, at which time the duty diving bends outcomes. DCS is a condition in which gas bubbles that form team (a specialized and trained group of divers and medical while diving do not have adequate time to be resorbed or “off- personnel who respond to diving casualties) was activated. The gassed.” This results in bubble entrapment in specific regions diver was promptly transported to the support team and diving of the body, most commonly in joints such as the shoulder. If chamber. When the diver arrived approximately five minutes adequate decompression time is omitted, the trapped bubbles later, the entire right side of his body was numb. He also had may lead to DCS.1 POIS is due to an overly rapid ascent to difficulty ambulating. The diver was urgently brought to the the surface resulting in the rupture of alveoli and subsequent hyperbaric chamber where he immediately descended to 60 extravasation of air bubbles into tissue planes.2 On rare occa- feet of seawater (fsw) and was placed on 100% oxygen. Within sions, the bubbles may traverse the cerebral circulation, causing minutes, the diver had full resolution of his symptoms. A full a potentially fatal condition.2 Divers must always be cognizant treatment per the US Navy standard diving guidelines was of dive time and depth, and be trained in the management of completed for the diagnosis of arterial gas embolism (AGE). decompression. A slow and controlled ascent, plus proper This scenario describes pulmonary barotrauma resulting in control of buoyancy can reduce the dangerous consequences arterial gas embolism. The diver’s rapid ascent to the surface of pulmonary barotrauma. Overall, the incidence of adverse after repeated dives placed the diver at increased risk for POIS. effects can be diminished with safe practices, allowing for the His symptoms were of quick onset and rapid progression, ulti- full enjoyment of this adventurous aquatic sport. mately requiring emergent treatment with hyperbaric oxygen therapy (HBO). Fortunately, he was in close proximity to a Relevance to Hawai‘i and Asia Pacific and had expeditious treatment. The Hawaiian Islands and islands throughout Asia Pacific are Following HBO treatment, the resolution occurred quickly popular scuba diving venues with an abundance of after he reached 60 fsw, which supports the diagnosis of arte- and warm, comfortable weather conditions year-round. The rial gas embolism. In AGE, air bubbles enter into the cerebral incidence of diving-related DCS ranges from 1 to 35 events circulation and become lodged in the arterial vasculature, result- per 10,000 dives, depending on region of the world and spe- ing in symptoms mimicking a stroke. HBO therapy essentially

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 13 follows Boyle’s Law, wherein the increase in atmospheric the volume and pressure will vary in such a way that the prod- pressure causes the volume of the bubble to decrease, allowing uct of the pressure and volume will remain constant.2 In other for circulation to be restored. words, on ascent, when the is decreasing, the volume of gas bubbles will increase (P1V1 = P2V2). This Case 2 explains why pulmonary barotrauma occurs. Inexperienced A 35-year-old man was in the process of becoming certified as divers who panic may ascend rapidly and develop POIS. an advanced scuba diver with a dive company from O‘ahu. He is the most serious manifestation of POIS, was to complete multiple dives, including wreck and night dives. resulting from gas passing from the ruptured lung into the The first day, he completed a dive for thirty-five minutes to 65 pulmonary veins and then into systemic circulation. Here, it feet, followed by another dive that night for thirty minutes to 45 can cause vascular damage or obstruction, hypoxia, infarction, feet. The diver felt well and the following morning joined his and activation of an inflammatory cascade. Initial presentation dive crew for his third dive of the weekend. He made a dive to includes loss of consciousness or symptoms similar to acute sixty feet for 45 minutes. The fourth dive, two hours later, had stroke. The symptoms upon ascent are often immediate, but been planned to a maximum depth of fifty feet. The diver was may present up to ten minutes after surfacing. Serious effects feeling very tired with pain in his right shoulder. Despite his may result from blockage of cerebral or coronary vessels by symptoms, he continued with his final dive. Surprising to him, bubbles merely 25 to 50 microns in diameter, or by interrupt- when he reached depth, his shoulder pain resolved. However, ing flow. Treatment must be immediate, consisting of urgent when he reached the surface after this final dive, his shoulder recompression in a hyperbaric chamber.1 pain recurred. This diver did not state any complaints after his The three types of pulmonary barotrauma are typically less dive course and went home. His wife noted that her husband serious, but may warrant treatment. The mechanism is similar was acting more fatigued than usual and perhaps had some ele- to the pathophysiology of pulmonary barotrauma. After alveo- ment of and memory loss. Furthermore, he began to lar rupture, gas escapes into the interstitial pulmonary tissues. complain of worsening shoulder pain. The following day, the This gas may track along the loose tissue planes surrounding diver presented for medical advice, examination and possible the airways and blood vessels, into the hilar regions, and then treatment. His symptoms raised the suspicion for DCS, even into the mediastinum, neck and the pleural space. This results though his did not show any “omitted decom- in mediastinal emphysema, or pneu- pressions” during his dives. Omitted decompression occurs mothorax. Symptoms include voice changes, feeling of fullness when a diver fails to make a needed decompression stop. Dive in the throat, dyspnea, dysphagia, retrosternal discomfort, chest computers are programmed to indicate when decompression pain, or in extreme cases, syncope and collapse. As in the case stops are required and the duration of these stops. Since DCS of emphysema, crepitus is often palpated on the surface of the was suspected, he was treated in the hyperbaric chamber, and skin. Usually these syndromes are self-limited and treated with his symptoms resolved after two days of HBO therapy. observation, allowing time for resorption of the gas bubbles. This diver likely suffered from decompression sickness, Mild symptoms may be treated with 100% oxygen administered which may be seen in divers who adhere to their dive time and by face mask for approximately 4-6 hours. In severe, albeit rare depth and do not omit decompression. Interestingly, this diver cases, a shallow decompression treatment may be started, which had an echocardiogram with agitated saline which revealed a is usually adequate for resolution. Pneumothorax may require Patent Foramen Ovale (PFO). It is unclear whether the PFO chest tube placement, depending on the size and symptoms contributed to his DSC. present.1,2 Decompression sickness is much more common. Present-day Discussion diving often follows dive tables, initially adopted by the US Diving compressed gases (ie, scuba diving) can lead to two very Navy. Modern technology allows for most divers to use dive serious medical conditions: Decompression Sickness (DCS), computers which can track their dive and decompression time otherwise known as “the Bends,” and Pulmonary Over-Inflation accurately, without having to calculate diving time based on Syndrome (POIS). DCS most often is not lethal, but is associ- depth and the dive tables. Despite advances with dive comput- ated with morbidity, whereas POIS can result in a spectrum of ers, divers still develop DCS, either from human error or from disorders from minor complaints to potentially lethal sequelae disobeying their decompression guidelines. Even if a diver is unless emergent treatment with hyperbaric oxygen therapy is adherent to appropriate dive time and depth, the dive tables are performed. not infallible and DCS may still occur. There are four distinct disorders as a part of POIS: Arterial gas During DCS, there is liberation of gas bubbles from embolism (AGE), pneumothorax, mediastinal emphysema and into the tissue or blood. Symptoms often resolve, but, these subcutaneous emphysema. They all result from overdistention bubbles may lead to death or permanent neurological impair- and rupture of the lungs by expanding gases during ascent.1,2 The ment. Bubbles may cause direct mechanical effects such as tissue expanding gases cannot escape, leading to one of the myriad of distortion or disruption, or ischemia by blocking blood vessels symptoms of POIS. Boyle’s law states that if the temperature or increasing tissue pressure sufficient to impair . of a fixed mass of gas is kept constant, the relationship between They are also known to precipitate an inflammatory cascade

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 14 via neutrophilic activation as a consequence of endothelial an increased risk to any of the divers or crew; (3) the diver or cellular damage.1,2 Basically, when diving, the deeper the with DCS is stable, without any altered state and has ability depth, the greater the partial of gases, which leads to use his or her extremities without additional risk; and (4) to an increase in bubble formation/extraction into the tissues. enough air and tanks are available for in-water decompression. The longer one remains at that depth, the more bubbles will One may try to use 100% oxygen underwater, if available, but “on-gas.” The ability of these bubbles to become resorbed into there MUST be another diver closely monitoring for oxygen solution, or “off-gas” will depend on how many gas bubbles , and the diver should not be at a depth greater than 30 have accumulated, which depends on time and depth. Thus, feet of salt water (O2 toxicity risk is greatly increased when one is required to undergo decompression stops in order to submerged to depths greater than this). Another treatment for allow time for this “off-gassing” to occur. If decompression is austere environments includes 100% oxygen on the surface, omitted, the result may be decompression sickness. which may be beneficial as a bridge to more definitive therapy. Furthermore, the severity of DCS will also be determined by A final option is air evacuation to the closest treatment facility. the amount of omitted decompression. There are many theories Whenever diving operations are underway there always needs as to how DCS develops, but one unifying mechanism has not to be a plan for potential emergency situations, and the boat been established. It is a multifactorial and multiorgan process. operator needs to have radio and phone numbers available. There are established risk factors that may predispose a diver to developing decompression sickness. Lack of physical fitness, Treatment in Non-austere Environments increased age, obesity, dehydration, physical injury, use In diving areas where resources are available, treatment for DCS during diving, repetitive dives, and traveling to altitude to dive predominantly entails HBO therapy. However, if symptoms are are some of the risk factors that may lead to higher incidences mild, observation only is required. The stricken diver should still of DCS.1 The best outcomes after diving are in physically fit have expert consultation either by a diving medical specialist individuals who are well-hydrated and who follow their dive or by the nearest emergency room. tables or dive computers without pushing the limits. If a diver should surface with symptoms suggestive of severe Clinical manifestations are classified into two categories: barotrauma, severe DCS, or arterial gas embolism, all efforts Type I “pain only,” and Type II “serious.” Type I is more should be undertaken to transport the patient emergently to the common, often with limb or joint pain, and usually affecting nearest hyperbaric chamber. the shoulder.1,2 Classically, this pain is unaffected by range of motion testing, which differentiates it from musculoskeletal Conclusion trauma or injury. However, one must be cautious because old Scuba diving is an extremely popular sport, especially in the injuries are predisposed to developing DCS, acting as a nidus Hawai‘i. Many experienced divers as well as newly trained div- for bubble formation and trapping.1 In Type II, symptoms are ers flock to the region to experience the marine environment. A more serious and usually occur with a significant amount of moderate climate makes the sport popular throughout the year. omitted decompression or extreme deep and long dives. Cere- With the incidence of decompression illness approximating one bral, cerebellar, spinal, and inner ear DCS comprise the Type II DCS case per 1000 dives, we would expect at least one event sub-categories, with emergent decompression being necessary every week. These diving related disorders need to be recognized, to avoid death or long-term neurological defects.1 and supervisors and the divers should be cognizant of the risks Whether one is treating decompression sickness or pulmonary and dangers that can accompany any dive. Divers need to be overinflation, the mainstay of treatment is to recompress the well-trained, know their limits, follow their planned dive, and affected diver in a hyperbaric chamber with 100% oxygen at always have an emergency plan. high partial pressures. This immediately reduces bubble size, and produces an increased gradient of inert gas (usually Disclosures ) out of the bubbles.2 This leads to relief of ischemia The author reported no conflicts of interest. and hypoxia, and restores normal tissue function. As long as the chambers are operated by well-trained staff and measures Disclaimer are taken to mitigate any adverse effects from decompression The views expressed in this manuscript are those of the author therapy, HBO treatment has the potential to reduce mortality and do not reflect the official policy or position of the Department and morbidity in most cases of DCS. of the Army, Department of Defense, or the US Government.

Treatment in Resource Constrained Author’s Affiliation: Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 Environments In environments which are remote or where resources are limited, Correspondence to: divers who succumb to decompression sickness may undergo Jennifer Hall DO; Tripler Army Medical Center, Honolulu, HI 96859; Email: [email protected] in-water decompression, as long as the following parameters are met: (1) additional divers can assist the stricken diver and accompany them under water; (2) the sea state does not pose

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 15 References 3. . Web site, data on diving casualties; 2013. Available at www.diversalert- 1. Edmonds C, Lowry C, Pennefather J and Walker R. Diving and Subaquatic Medicine. New network.org. York, NY; 2002: 55-72, 131-166. 4. The incidences of decompression illness in 10 years of . Diving Hyperbaric 2. Bove A, Davis J. . W.B Saunders Company;1990:170-190. Med. Dec. 2012.

Alternobaric (Photo: Russell Gilbert MD)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 16 of Hawai‘i Volcanoes National Park

Gregory M. Sprowl MD

Introduction adults experience increased airway resistance at 5ppm, sneez- For the wilderness enthusiast, Hawai‘i is renowned as a safe ing and coughing at 10 ppm, and bronchospasm at 20 ppm.8 tropical destination free from snakes, diseases of the develop- Respiratory protection is required for exposures at or above ing world, and dangerous . One of the most popular 20 ppm.7 Sulfur dioxide exposure in the National Park varies destinations is Hawai‘i Volcanoes National Park. With over a widely depending on location and wind direction. With nor- million visitors per year, the park is one of the top fifteen visited mal northeasterly trade winds the most highly trafficked areas national parks in the United States.1 It possesses the only active such as the Visitor’s Center and Jagger Museum are likely to volcanoes, with unique hazards such as the terrain of established experience less than one ppm to zero sulfur dioxide exposure.9 lava flows, unstable lava deltas, lava, and volcanic gases. A Close to vent sites and several kilometers downwind, visitors visitor can sustain trauma, altitude related illness, burns, hyper can experience levels over 1 ppm and even over 100 ppm in and hypothermia, and exacerbation of existing lung conditions. very close proximity.9 Measurements up to 75 ppm have been recorded at lava coastal entry sites, locations which are par- Relevance to Hawai‘i and Asia-Pacific ticularly sought by visitors.9 Advancing lava has destroyed multiple communities on the Exposure to sulfur dioxide in large quantities has been island of Hawai‘i (Big Island) since Kilauea’s latest eruption documented to produce reactive airways dysfunction syndrome began in 1983.2 This has substantially altered the terrain, de- (RADS).10 RADS falls within the same spectrum of disease stroying infrastructure, and making it difficult to traverse by as irritant induced asthma, and can present as acute asthma in vehicle or foot.2 Vog, a mixture of sulfur dioxide (SO2) and individuals with no prior history after just a single high dose other gases emitted from a volcano reacting with oxygen in exposure. RADS can lead to long-term asthma-like symptoms sunlight, exacerbates respiratory and ocular conditions in sus- that persist for years. It is not well characterized histologically, ceptible individuals. Concentrated levels of SO2 above World and is not known to be immune mediated.10 In several studies Health Organization (WHO) recommended exposure levels of RADS, a majority of patients experienced symptoms fol- exist frequently on Hawai‘i island communities southwest of lowing methacholine challenge, and spirometry continued to Kilauea, downwind of the usual northeasterly trade winds.3 be abnormal over five years later. While most studies show a mild inflammatory response with sparse lymphocytes and Clinical Relevance granulocytes, there is an absence of eosinophilia, smooth muscle Kilauea, the more active of the two active shield volcanoes on hyperplasia or mucus gland hypertrophy that are characteristic Hawai‘i Island, has historically produced an average of over of asthma.10 100 tons per day of sulfur dioxide, the most abundant gaseous is also a colorless gas with a distinctive emission.5 In some of the more active years since 1983, rates rotten egg odor that is emitted in sizeable quantities from have exceeded 1,000 tons per day.3 In addition to sulfur dioxide, Kilauea.9 From May to September 1993, the maximum recorded considerable quantities of hydrogen sulfide, carbon dioxide, measurement of H2S was 4.23 ppm at Sulphur Banks, but from carbon monoxide, hydrochloric acid, and particulate matter are 1987-1990 measurements only rarely exceeded the Hawai‘i State produced. 6 These gases can produce acute effects on visitors Department of Health air quality limit of 0.025 ppm at the park with chronic respiratory and cardiac disease. monitoring site.9 OSHA total weighted average exposure limit 9 Traversing the terrain of the lava fields causes hundreds of for H2S is 10 ppm, with a short term exposure limit 15 ppm. At mechanical injuries each year, including lacerations, abrasions, above 20 ppm, exposure can elicit headaches, fractures, sprains, and strains.4 Additionally, dozens of thermal dizziness, nausea and eye irritation. Respiratory effects include burns have been recorded over the last twenty years, including bronchitis, rhinitis, and pulmonary edema.11 Studies indicate several fatalities.4 that hydrogen sulfide inhibits cytochrome oxidase (aa3) result- Sulfur dioxide is a colorless gas; however it is frequently ing in disruption of the electron transport chain and inhibition mixed with other gases and particulate matter. It has a strong of oxidative in the mitochondria.12 More recent odor which most people can detect at 0.3 to 1 ppm, and is ir- experiments have determined that greater toxicity may result ritating to the respiratory tract.7 OSHA limits on sulfur dioxide from the production of reactive oxygen and depletion 13 exposure are an eight hour total weighted average of 2 ppm and of glutathione. No recorded from H2S exposure have a short term (15 minutes) exposure limit of 5 ppm.7 Asthmatics occurred in Hawai‘i, although numerous deaths have occurred in can experience increased airway resistance with sulfur dioxide areas of volcanic activity in Japan and New Zealand.6 Hydrogen concentrations of less than 0.1 ppm when exercising. Healthy sulfide toxicity is primarily a concern of industrial exposure.14

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 17 This is a very small primary volcanic HC1 gas emission. It is in the late 1980s when he fell on uneven lava while at produced in greater quantities when lava exceeding 1,100 degrees night from the flow front to his car parked near Kalapana.19 In C interacts with chlorides in seawater, and is a component of March 2003, a man suffered a mix of first, second, and third the superheated steam plumes.9 While 1994 USGS ambient air degree burns over eight percent of his body when he fell into measurements recorded only one ppm of HCl at a coastal entry an active flow.16 point for lava within the park, this was skewed by the fact that In April 1993 a local native of the island of Hawai‘i, a Kona the measuring device only recorded gas, not aerosol vapor. The photographer, died at Kilauea’s Eruption Site when a lava bench pH of rain water sampled at the same site supports the theory which appeared to be solid collapsed.21 He was attempting to that the HCl measured levels are not an accurate indication of photograph the entry site of lava into the ocean. He and several total HCl .9 OSHA has a permissible exposure other onlookers had crossed a rope barrier set up by park rang- limit of 5 ppm established. Exposures to 35 ppm causes throat ers. When the bench collapsed, the others were able to scramble irritation and, with higher concentrations over time, can result to safety, but Nagar was swept into the sea. Five years later, in in swelling and spasm of the throat and bronchospasm. The April 1998, a hiker was declared lost at sea after an extensive resulting endothelial damage at high exposure levels may lead search when he slid off a coastal cinder cone at the ocean edge. to pulmonary edema, progression to acute respiratory distress This occurred at approximately 1 a.m. when the group with syndrome (ARDS), and may induce RADS.15 whom he was hiking crossed a warning barrier.22 While exposure to gases poses a risk and has produced injuries and fatalities, most injuries and fatalities are caused by motor Treatment in Resource-Constrained vehicles on the roadways or air travel accidents.4 These caused Environments 178 of 262 park fatalities during 1993 to 2002.4 Other causes Persons entering the backcountry remote areas should ensure of death from this period during a study of park hazards indi- avoidance of areas with significant concentrations of toxic cated that thermal burns, heat stroke, cardiac arrest, respiratory gases by using basic information provided by the National distress, and mechanical injury rounded out the remainder.4 Park Service. This is particularly important for individuals with pre-existing asthma, COPD, or interstitial lung disease. Patients Example Cases with pre-existing conditions should carry an adequate supply From 1983 to 2003, five deaths of tourists were directly due of their control medications and avoid high-risk areas. Guides to SO2 exposure, with few details available. One person had a should consider carrying spare inhalers with a quick-acting history of asthma. The other four deaths occurred when these beta-agonist and possibly an inhaled corticosteroid. Mechanical individuals ignored warning signs for off-limits areas marked injury or dehydration are the most likely situations requiring during periods of elevated volcanic activity.6 A closer study medical care in the park. Individuals should be advised to pre- from 1993 to 2002 indicated that there were 28 asthma and pare their skin for sun exposure, travel with water, wear proper respiratory distress related deaths, but these were not attributed footwear, and maintain an ability to contact help should such to a single gas at the eruption site of Kilauea.4 an injury prevent self-evacuation.4 Additionally, visitors into On November 5, 2000, a woman, age 41, of Volcano, Hawai‘i, the backcountry should register with the park service before and a man, 42, of Washington, DC, were found dead near the venturing into less trafficked areas of the park.4 lava flow front entry into the ocean.16 They were found with The levels of gas exposure frequently experienced by hikers severe burns, cuts and abrasion to their heads, hands, and knees.17 and outdoor enthusiasts on Kilauea are not likely to harm an According to the medical examiner, “the two died as a result able-bodied individual. It is unlikely the victim or first responder of pulmonary edema caused by inhalation of steam sustained will be able to identify the exact gas that is the offending agent when exposed to a steam plume.”17 While the investigation in the field without specialized equipment. Therefore, treatment did not elaborate further regarding the specific etiology of the should focus on maintaining the airway and delivering oxygen. pulmonary edema, hydrochloric acid and superheated water The treatment for exposure to sulfur dioxide is similar to an steam itself are possible causes of such injuries. Of note, the acute asthma attack.7 Manifestations can include coughing, summary reported advanced decomposition of the bronchospasm, upper airway edema, acute lung injury, and exposed skin due to acid rain.18 death at exposures above 20ppm.7 First line treatment includes While relatively uncommon, thermal burns have caused high immediate removal from the exposure, use of an inhaled beta-2 profile injuries and fatalities in the park.4 In October 2002, a agonist and oxygen support. An emergency room visit is indi- cruise ship passenger, age 45, was found dead just north of the cated for observation or further treatment.8 There is minimal ranger station at the end of Chain of Craters Road.19 There were risk of secondary exposure to first responders once the patient no obvious injuries, foul play was ruled out, and she was not is out of the contaminated environment.8 found in immediate proximity to active lava flows. However, it For HCl exposure, secondary contamination of the rescuer was later reported that she was found twenty feet into a cooling is not a concern if the victim is dry; moist contaminate could lava flow.20 The official autopsy report declared that she died expose the rescuer to vapor.15 Skin or eye irritation should be of natural causes due to exposure.16 A lawsuit brought against a decontaminated with removal of clothing and thorough washing tour company that transported her to the park mentioned burns with soap and water.15 to her feet and other skin surfaces.20 A visitor from Japan died

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 18 Treatment in Non-Austere Environments increase afterload.25 ARDS is a documented consequence of There is no direct antidote for sulfur dioxide toxicity. Treatment HCl toxicity that requires extensive supportive care time and consists of support of respiratory and cardiovascular functions. resources. Treat bronchospasm with immediate acting aerosolized bron- Treat carbon dioxide and monoxide poisoning with supple- chodilators such as aerosolized beta-2-agonists.7 Additional mental oxygen. The half life of COHb at room air is five hours.26 treatment includes long acting aerosolized beta-2-agonists, Normal COHb levels in the blood are 1-3%, and can be increased IV and inhaled corticosteroids, oxygen and even intubation as in smokers up to 5-10%. Levels measured above this on an the clinical picture dictates. The use of aerosolized 2% sodium arterial blood gas require supplemental 100% oxygen therapy, bicarbonate solution has been documented as a successful treat- which will reduce the half life of COHb to 74 minutes.26 Ac- ment and is a consideration in more concentrated exposures.23 cording to Center for Disease Control (CDC) guidelines, COHb In theory, this helps neutralize and prevent the formation of levels above 25% or the presence of cardiac or neurological sulfurous acid and breakdown products which are involved in impairment are indications for hyperbaric O2 therapy, which bronchoconstriction.23 is the gold standard for care and reduces COHb half life to 25 For eye irritation due to sulfur dioxide exposure, remove any minutes.26 A literature search did not find the levels of COHb contact lenses and flush the eyes for at least fifteen minutes. or subgroups of victims that would most likely benefit from For skin exposure, flush skin with water for fifteen minutes, hyperbaric oxygen therapy.27 removing from contact any contaminated clothing and shoes. The clothing and shoes may be washed thoroughly and reused.7 Conclusion Patients without pulmonary complaints in a 6- to 8-hour ob- While volcanic gas and lava flow injuries are important, the servation period are not likely to develop complications. They vast majority of park injuries are due to motor vehicle accidents may be released and advised to rest and to seek medical care and man-made hazards. Most of the over one million tourists promptly if symptoms develop.7 For symptomatic patients, the to Hawai‘i Volcanoes National Park report no incidents at all. injury may evolve over the course of 18 to 24 hours depending If the visitor is properly equipped, conditioned, realistic about on the level of exposure and co-morbidities of the patient.7 their health, and willing to follow the signs, they will likely Treatment for acute hydrogen sulfide toxicity begins with avoid becoming a story in a newspaper. In a 2004 survey of 800 supportive care: removal from the offending site, administration hikers leaving the lava fields, which often involves a 10-plus of oxygen and suctioning of secretions.14 Antidotes to consider kilometer hike to view active lava, 93% of respondents admit- if hypoxia is not readily corrected with oxygen include those ted hiking beyond warning signs posted 500 meters from the which will induce methemoglobinemia such as high dose in- eruption site where the lava meets the ocean. Over half were ill haled amyl nitrate and IV sodium nitrate.14 Inhaled amyl nitrite prepared, defined as lacking flashlights, sufficient water, first should be avoided if the individual is hypotensive, because a aid kits, and sunscreen.18 Many had pre-existing health issues, primary mechanism of action is cardiac and peripheral smooth including heart problems and asthma.18 muscle relaxation. Ten mL of 3% IV sodium nitrite over two It is prudent to remember to use vehicle safety measures, a to four minutes, and IV pyridoxine are more likely to be more hydration plan, protection from the sun, and proper footwear effective in inducing the desired methemoglobin state.12 The when traversing terrain by foot. Individuals with pre-existing methemoglobin production will scavenge the offending sulfide respiratory and cardiac conditions should have a supply of species, forming a transient sulfmethemoglobin species with a , minimize physical stress, and consult the air qual- half life of two hours at 24 degrees Celsius which will further ity guide for the park at http://www.hawaiiso2network.com/ decay into oxyhemoglobin and an oxidized form of sulfur.12 managed by the US Geological Survey. Finally, obey all signs Other treatments to consider include hyperbaric oxygen and placed by park personnel that warn visitors of hazards such as therapeutic red cell exchange.14 unstable terrain and high levels of toxic gases. The mechanism of hydrochloric acid toxicity is due to corrosive effects and the formation of free radicals causing Disclosure parenchymal damage to the lung.24 The care is supportive. The author reported no conflicts of interest. Bronchodilators may be required to counteract bronchospasm.24 Non-invasive ventilation devices may be required to maintain Disclaimer oxygen saturation and intubation may be required. For pulmo- The views expressed in this publication are those of the author nary edema, in addition to oxygen support, loop diuretics are and do not reflect the official policy or position of the Department the drug of choice, with furosemide having the added benefit of the Army, Department of Defense or the US Government. of venodilation effects, reducing preload. For furosemide, start with a dose of 0.5mg/kg, up to 1mg/kg for renal insufficiency or Author’s Affiliation: Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 chronic use.25 Other agents that reduce preload, such as nitrates, are also effective as long as is not present Correspondence to: or induced. Morphine also induces venodilation and relieves Gregory M. Sprowl MD; Tripler Army Medical Center, Honolulu, HI 96859; Email: [email protected] dyspnea and while reducing catecholamine effects that

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 19 References 16. Dayton K. Tourist falls into lava. Honolulu Advertiser. Mar 11, 2003. http://the.honoluluadvertiser. 1. La J, Netburn D. The 20 most visited national parks in the U.S. Los Angeles Times. http:// com/article/2003/Mar/11/ln/ln10a.html. Accessed November 29, 2013. www.latimes.com/travel/la-tr-top20nationalparks-pg,0,4023261.photogallery#axzz2mMJcIx3e. 17. Viewing Lava Safely-Common Sense is Not Enough! US Geological Survey Hawaiian Volcano Accessed December 2, 2013. Observatory Web Archive. http://hvo.wr.usgs.gov/archive/2000_11_15.html. Updated April 9, 2. Thompson R. Mixed blessing. Honolulu Star-Bulletin. January 1, 2003. http://archives.starbul- 2001. Accessed November 23, 2013. letin.com/2003/01/01/news/index9.html. Accessed October 3, 2013. 18. Pratt SE. Danger in paradise: The hidden hazards of volcano geotourism. Earth. 2012. http:// 3. Longo, BM. The Kilauea Volcano Adult Health Study. Nursing Research. 2009;58(1):23-31. www.earthmagazine.org/article/danger-paradise-hidden-hazards-volcano-geotourism. Ac- 4. Heggie TW. “The epidemiology and etiology of visitor injuries in Hawaii Volcanoes National cessed November 29, 2013. Park” [PhD thesis]. College Station, TX: A&M University; 2005. 19. Advertiser Staff and News Services. No signs lava caused park death. Honolulu Advertiser. 5. Elias T, Sutton AJ. Sulfur Dioxide Emission Rates from Kīlauea Volcano, Hawaii, an Update: October 17, 2002. http://the.honoluluadvertiser.com/article/2002/Oct/17/ln/ln19a.html. Accessed 2002-2006. Reston, VA: US Geological Survey; 2007. Open-File Report 2007-1114. 3 October 2013. 6. Hansell A, Oppenheimer C. Health hazards from volcanic gases: a systematic literature review. 20. Gast v. Kwak, 396 F. Supp. 2nd 1150 (D. Hawaii 2005). Archives of Environmental Health. 2004;59:628-639. 21. Dayton K. Massive outcropping of fresh lava may collapse. Honolulu Advertiser. August 20, 7. Toxicological profile for sulfur dioxide. Agency for Toxic Substances and Disease Registry Web 2005. http://the.honoluluadvertiser.com/article/2005/Aug/20/ln/FP508200352.html. Accessed Site http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=253&tid=46. Accessed December 2, 2013. 5 October 2013. 8. The Center for Research Information, Inc. Health effects of Project SHAD chemical agent: sulfur 22. Star-Bulletin staff. Searchers can’t find volcano hiker who fell.Honolulu Star-Bulletin. April 30, dioxide. Silver Spring, MD: The National Academies; 2004. Contract No. IOM-2794-04-001. 1998. http://archives.starbulletin.com/1998/04/30/news/briefs.html. Accessed 23 November 9. Sutton AJ, Elias T, Navarrete R. Volcanic gas emissions and their impact on ambient air 2013. character at Kilauea Volcano, Hawaii. Reston, VA: U.S. Geological Survey; 1994. Open-File 23. Barach, AL. Treatment of sulfur dioxide poisoning. JAMA. 1971;215:485. Report 94-569. 24. Bansal DP, Ambegaonkar R, Radhika P, Sharma M. ARDS following inhalation of hydrochloric 10. Patel DP, Patel RK, Patel NJ. Review on reactive airways dysfunction syndrome (RADS). Asian acid. Journal of the Association of Physicians of India. 2011;59. http://www.japi.org/february_2011/ J Pharm Clin Res. 2012;5(suppl 3): 10-15. article_10.html. Accessed November 29, 2013. 11. Medical management guidelines for hydrogen sulfide. Agency for Toxic Substances and Dis- 25. Hochman, JS, Ingbar, DH. Cardiogenic and pulmonary edema. In: Fauci AS, Braunwald ease Registry Web Site. http://www.atsdr.cdc.gov/mmg/mmg.asp?id=385&tid=67. Accessed E, Kasper DL et al, eds. Harrison’s Principles of Internal Medicine. 17th ed. New York: McGraw- December 2, 2013. Hill Medicine; 2008: 1702-1707. 12. Smith, RP, Gosselin RE. Hydrogen sulfide poisoning. Journal of Occupational Medicine. 26. Clinical guidance for carbon monoxide (CO) poisoning after a disaster. Centers for Disease 1979;21(2)93-97. Control and Prevention Web Site. http://emergency.cdc.gov/disasters/co_guidance.asp. Updated 13. Truong DH, Eghbal MA, Hindmarsh W, Roth SH, O’Brien PJ. Molecular mechanisms of hydrogen September 19, 2008. Accessed November 29, 2013. sulfide toxicity. Drug Metab Rev. 2006;38(4):733-744. 27. Wolf SJ, Lavonas EJ, Sloan EP et al. Clinical Policy: Critical issues in the management of adult 14. Doujaiji B, Al-Tawfiq JA. Hydrogen sulfide exposure in an adult male. Ann Saudi Med. patients presenting to the emergency department with acute carbon monoxide poisoning. Ann 2010;30(1):76-80. Emerg Med. 2008;51:138-152. 15. Medical management guidelines for hydrogen chloride. Agency for Toxic Substances and Dis- ease Registry Web Site. http://www.atsdr.cdc.gov/mmg/mmg.asp?id=758&tid=147. Accessed December 2, 2013.

Halema‘uma‘u Crater Caldera at Kilauea (Photo: Russell Gilbert MD)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 20 Leptospirosis: The Microscopic Danger in Paradise

William A. Londeree MD

Abstract Leptospirosis is a zoonotic infection endemic in Hawai‘i. This review discusses of Australis is most likely related to the increasing the incidence of documented human cases in Hawai‘i and current recommen- population and interactions between feral swine and humans.2 dations for diagnosis, prevention, and treatment of leptospirosis. Example Case Introduction A 21-year-old man with no prior significant medical history While vacationing or living in paradise, the last thought to pass presented to the emergency department with progressive nausea through a person’s mind is the possibility of contracting a seri- and headache over the past week. Onset occurred one week after ous or life-threatening bacterial illness like leptospirosis after at Maunawili Falls. He started having periumbilical a quick dip at a beautiful waterfall or a hike near a picturesque pain and became intolerant of oral intake due to persistent nausea. stream. Leptospira interrogans is a freshwater-borne zoonotic Non-bloody, non-bilious emesis was followed by brown, watery spirochete capable of infecting a variety of mammalian hosts to and a subjective fever. Initial vital signs demonstrated a include cattle, swine, goats, and rodents, but rodents and feral temperature of 103.3°F, blood pressure of 110/66 mm Hg, heart swine mainly serve as carriers in Hawai‘i. Once the infection rate of 95 beats per minute, of 18 per minute, has occurred in these carrier animals the spirochete will be shed and oxygen saturation of 100% on room air. Physical exam intermittently in the urine where it will remain viable for days was only remarkable for mild diffuse abdominal tenderness to months in soil or water with a neutral pH.1,2 without hepatosplenomegaly or peritoneal signs. Diagnostic The infection in humans can range from a subclinical infection laboratory studies demonstrated elevated C-reactive protein, to severe multi-organ failure. Leptospirosis has an incubation erythrocyte sedimentation rate, and aspartate aminotransferase. period of 2 to 26 days and classically presents with , rig- A normochromic normocytic anemia, thrombocytopenia, and ors, myalgias, and headaches in 75 to 100 percent of patients.1,2 leukocytosis were also present. He was admitted to a telemetry Given its variability in clinical presentation, leptospirosis can ward and treated with ciprofloxacin for a suspected bacterial be a difficult disease to diagnose, so it is usually treated empiri- diarrheal illness and intravenous doxycycline for a possible cally when suspected. Medications and preventive stategies can leptospirosis infection. Four hours after the administration of decrease the likelihood of acquiring the systemic infection. antibiotics he developed respiratory distress and had to be intu- bated for hypoxic . A chest X-ray demonstrated Relevance to Hawai‘i pulmonary edema, and shortly after intubation he developed Leptospirosis is endemic worldwide, but the majority of in- bloody sputum which was suctioned through his endotracheal fections occur in the tropical regions with Hawai‘i reporting tube. Diffuse alveolar opacities were seen on CT scan, and the highest incidence of human cases in the United States. bronchoscopy with a bronchoalveolar lavage demonstrated only The Hawai‘i Department of Health reported 345 cases to the gross red blood cells consistent with diffuse alveolar hemorrhage. CDC in Hawai‘i with 198 cases confirmed from 1999-2008.2 He was extubated after three days of mechanical ventilation and Most of the 91% confirmed cases occurred in men, and 71% discharged three days later. Microscopic agglutination testing of these cases occurred in the age range of 20-49 years. Nearly demonstrated a positive, 1:800 IgM antibody titer for Leptospira 80% of these cases were due to freshwater exposure from interrogans serovar Icterohemorrhagiae. At follow-up, he had outdoor recreational activities or taro farming. The remaining made a complete recovery. 11% percent of exposures were from home gardens.2 Since the incidence of infection in Hawai‘i is higher than the rest Presentation and Diagnosis of the United States, and the main risk factor for leptospirosis Cases of leptospirosis can range from a mild or subclinical is exposure to freshwater and moist soil, infection rates may infection to a very severe and potentially fatal one. Most mild decrease if people are educated on use of appropriate personal cases usually present with fevers, myalgias, and headache protection equipment, avoidance of freshwater exposure, and similar to an acute viral febrile illness, but severe cases can pharmacologic prophylaxis. present with jaundice, renal failure, hemorrhagic diathesis, The most common infecting serovars are from serogroups anemia, hyponatremia, hypokalemia, and thrombocytopenia.2, 3 Icterohemorrhagiae (40%) and Australis (44%), which have Diagnosis of leptospirosis relies on a detailed history and been shown to have predominantly rodent and swine carriers, clinical suspicion, because the current testing modalities have a respectively. In the past, serogroup Icterohemorrhagic was re- long turnaround time and are not clinically useful in an acutely sponsible for the majority of infections, but the increasing rate ill patient. The gold standard test is the microscopic agglutina-

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 21 tion test (MAT), which uses antigens from live spirochetes from endemic areas and in areas after natural disaster where flooding multiple serogroups and mixes them with a patient’s serum to or contaminated bodies of water are present.15 detect concentrations of agglutinating antibodies. One downfall Exposure to freshwater or moist soil which has been con- of this test is its prolonged turnaround time. Another downfall taminated with spirochetes from infected mammalian urine is of the MAT is the requirement for maintenance of live cultures a major risk factor for contracting leptospirosis. Humans can of Leptospira which are endemic to the local area. Also, a single help prevent infection by avoiding exposure to stagnant water, MAT test cannot differentiate between a current or recent prior properly draining farm water runoff, and keeping food away infection, and there is cross reactivity with other previous from waste contamination. Vaccination of domestic spirochete infections.4 Titer range for test positivity is open to animals has been extremely effective; however, some immu- debate, but is typically set at a value > 1:200. Enzyme-linked nized animals still acquire the infection and shed spirochetes immunosorbent assay (ELISA) is another test showing promise in their urine because the infection resides in the renal tubules. because it is able to detect an earlier rise in IgM antibodies. These carriers must be treated with therapy in order to The test has variable specificity and sensitivity due to operator clear their infection but this is not practical due to the animals expertise, so it is currently not recommended.2,5,6 Polymerase continued exposure to leptospirosis.16 chain reaction (PCR) is another test undergoing development Several control measures are available for humans. Prevention but it is best when it is utilized in conjunction with ELISA. education in high risk areas is important. Controlling the disease Combining ELISA for IgM detection, followed by PCR to in domestic animals by vaccination is useful. Additional mea- detect the antigen in the blood or in the urine to confirm an sures include limiting exposure to feral swine, rodent control, active infection, is currently being evaluated.7,8 and protection of food from animal contamination (either do- mestic or feral). Doxycycline is available as chemoprophylaxis Prevention for people at increased risk of exposure.15 Prevention starts with avoiding high risk exposures to infected water sources. There are roles for chemoprophylaxis and vac- Treatment cination of animals; however, there is no currently approved The clinical efficacy of antimicrobials in a mild leptospirosis human vaccine for use in the United States. infection is not well established and remains a topic of contro- Vaccination faces many challenges because leptospirosis has versy. A meta-analysis demonstrated that there may be decreased more than 200 pathogenic serovars. China and France are the duration for the clinical illness by 2-4 days, but the results were only countries that have a vaccine available for human use. A not statistically significant.17 Given the risks associated with difficulty with developing an efficacious vaccine is matching the the severe form of infection, a patient should be treated with local serovars to the vaccine. Limited safety data are available appropriate antibiotic therapy as soon as possible, preferably on human use.9, 10 Even though there is no vaccination available within five days of symptom onset.15 for residents of Hawai‘i, pharmacological prophylaxis strategies Penicillin is recommended for a severe leptospirosis infec- are available. tion by the World Health Organization (WHO), but usually The United States Army assessed 940 US soldiers during stronger antibiotics are given in the hospital in order to broaden deployed jungle training in Panama with doxycycline pro- coverage. Worldwide, leptospirosis has not demonstrated a phylaxis 200 mg a week orally versus a placebo. The soldiers pattern of resistance, and it is susceptible to a large variety of receiving doxycycline had an infection rate of 0.2% compared antibiotics. Antimicrobial activity against leptospirosis has been to a 4.2% infection rate experienced by the placebo group, yield- observed during in vitro studies with penicillins, cephalosporins, ing an efficacy of 95%.11 Since the soldiers were likely a naïve tetracyclines, chloramphenicol, fluoroquinolones, macrolides, population, studies have also been conducted on indigenous telithromycin, carbapenems, and aztreonam. In 2008, Ress- populations to assess prophylaxis efficacy. Two studies assessed ner, et al, published a comprehensive review of antimicrobial indigenous populations from Brazil and North Andaman with susceptibilities in different geographic regions. Overall, the doxycycline prophylaxis (200mg weekly) versus placebo. The study analyzed 13 Leptospira isolates from Egypt, Thailand, Brazilian study found a protective association with doxycycline Nicaragua, and Hawai‘i. Among thirteen antimicrobial agents and seroconversion, but it was a small pilot study and did not tested, ampicillin, cefepime, azithromycin, and clarithromycin demonstrate statistical significance.12 The study from North had the lowest MICs (< 0.016mcg/ml), with slightly higher Andaman included 782 persons and it revealed an infection rate MICs recorded for cefotaxime, ceftriaxone, imipenem-cilastatin, of leptospirosis was not statistically different from the placebo penicillin G, moxifloxacin, ciprofloxacin, and levofloxacin group, however, there was a significant protective effect in (0.030- 0.125 mcg/ml). Overall, the highest MICs were for reducing morbidity and mortality in the doxycycline group.13 doxycycline and tetracycline at 2.0 and 4.0, respectively, for In contrast to these studies, a systematic review conducted in strains obtained in Egypt. Icterohemorrhagiae was the Hawai- 2000 did not demonstrate certainty for leptospirosis prevention ian serovar analyzed in this study and its MICs to doxycycline with doxycycline, but it could not make an argument against and tetracycline were the highest when compared to the other prophylaxis.11, 14 The World Health Organization recommends antibiotics at 0.50 and 1.00, respectively.18 physicians consider using prophylactic doxycycline in highly Most cases of leptospirosis are subclinical and will never

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 22 undergo antibiotic treatment. However, for adult patients with References 1. Kaufmann, AF, Weyant, RS. Leptospiraceae. In: Manual of Clinical Microbiology, 6th ed, ASM mild disease who are candidates for outpatient therapy, doxy- Press, Washington, DC, 1995, p. 621. cycline or azithromycin are accepted treatments. Children and 2. Katz AR, Buchholz AE, Hinson K, Park SY, Effler PV. Leptospirosis in Hawaii, USA, 1999–2008. Emerging Infectious Diseases. 2011Feb;17(2):221-226 pregnant women can be treated with amoxicillin or azithromycin 3. Katz AR, Ansdell VE, Effler PV, Middleton CR, Sasaki DM. Assessment of the clinical presenta- (for those with beta-lactam ) in order to avoid use of tion and treatment of 353 cases of laboratory-confirmed leptospirosis in Hawaii, 1974-1998. Clin Infect Dis. 2001;33(11):1834. doxycycline. 4. Guerra MA. Leptospirosis: Public health perspectives. Biologicals. 2013 Sep;41(5):295-7. When a patient has a more severe presentation of leptospi- 5 . Tanganuchitcharnchai A, Smythe L, Dohnt M, Hartskeerl R, Vongsouvath M, Davong V, Lattana O, Newton PN, Blacksell . Evaluation of the Standard Diagnostics Leptospira IgM ELISA for rosis requiring hospitalization, intravenous antibiotics such diagnosis of acute leptospirosis in Lao PDR. Trans R Soc Trop Med Hyg. 2012 Sep;106(9):563-6. as penicillin, doxycycline, ceftriaxone, or cefotaxime should 6. Desakorn V, Wuthiekanun V, Thanachartwet V, Sahassananda D, Chierakul W, Apiwattanaporn 15 A, Day NP, Limmathurotsakul D, Peacock SJ. Accuracy of a commercial IgM ELISA for the be administered. Upon initiation of antibiotic therapy there diagnosis of human leptospirosis in Thailand. Am J Trop Med Hyg. 2012 Mar;86(3):524-7. is a risk a severely infected patient could develop a Jarisch- 7. Picardeau M, Bertherat E, Jancloes M, Skouloudis AN, Durski K, Hartskeerl RA. Rapid tests for diagnosis of leptospirosis: current tools and emerging technologies. Diagn Microbiol Infect Herxheimer reaction (JHR). The JHR is hypothesized to be Dis. 2014 Jan;78(1):1-8. secondary to an acute inflammatory response caused by a large 8. Budihal SV, Perwez K. Leptospirosis diagnosis: competancy of various laboratory tests. J Clin Diagn Res. 2014 Jan;8(1):199-202. amount of cytokines released during clearance of spirochetes 9. Guerra MA. Leptospirosis: Public health perspectives. Biologicals. 2013 Sep;41(5):295-7. from the circulation. This reaction typically occurs within 1-4 10. Wang Z, Jin L, Wegrzyn A. Leptospirosis vaccines. Microb Cell Fact. 2007 Dec 11;6:39. 11. Takafuji ET, Kirkpatrick JW, Miller RN, Karwacki JJ, Kelley PW, Gray MR, McNeill KM, Timboe HL, hours after initial antibiotic administration and is commonly Kane RE, Sanchez JL. An efficacy trial of doxycycline chemoprophylaxis against leptospirosis. manifested by hypotension, rigors, fevers, and tachycardia, but N Engl J Med. 1984;310(8):497. 12. Gonsalez CR, et al. Use of doxycycline for leptospirosis after high-risk exposure in Sao Paulo, may also include respiratory distress and renal failure. No one Brazil. Revista do Instituto de Medicina Tropical de Sao Paulo 1998;40:59–61. antibiotic has been shown to have a higher association with 13. Sehgal SC, et al. Randomized controlled trial of doxycycline prophylaxis against leptospirosis in an endemic area. International Journal of Antimicrobial Agents. 2000;13:249–255. JHR. Patients should be closely monitored for the JHR after 14. Guidugli F, Castro AA, Atallah AN. Antibiotics for preventing leptospirosis. Cochrane Database initiation of antibiotic therapy.19 Syst Rev. 2000;(4):CD001305. 15. Human leptospirosis: guidance for diagnosis, surveillance and control. Geneva, World Health Organization/ International Leptospirosis Society, 2003. Conclusions 16. Martins G, Lilenbaum W. Leptospirosis in sheep and goats under tropical conditions. Trop Anim Health Prod. 2014 Jan;46(1):11-7. The best way to avoid a leptospirosis infection is through 17. Brett-Major DM, Coldren R. Antibiotics for leptospirosis. Cochrane Database Syst Rev. avoidance of areas of water and moisture which are exposed 2012;2:CD008264. 18. Ressner RA, Griffith ME, Beckius ML, Pimentel G, Miller RS, Mende K, Fraser SL, Galloway to feral animals, especially swine and rodents. Patients should RL, Hospenthal DR, Murray CK. Antimicrobial susceptibilities of geographically diverse clinical be educated by their primary care provider about contact human isolates of Leptospira. Antimicrob Agents Chemother. 2008 Aug;52(8):2750-4. 19. Guerrier G, D’Ortenzio E. The Jarisch-Herxheimer reaction in leptospirosis: a systematic review. avoidance. Prophylaxis with weekly oral doxycycline should PLoS One. 2013;8(3):e59266. be considered for individuals when exposure is unavoidable. Individuals who elect to forego prophylactic antibiotics should be counselled to seek immediate medical attention if they start feeling ill after an exposure to freshwater. Initiation of antibiotic therapy should be based on history, physical exam findings, and laboratory results that are consistent with possible leptospirosis infection. Patients with moderate to severe infections should be hospitalized for antibiotic therapy in a setting where they can be closely monitored for the development of serious systemic disease or a Jarisch-Herxheimer reaction.

Disclosure The author reported no conflicts of interest.

Disclaimer The views expressed in this abstract/manuscript are those of the author and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the US Government.

Acknowledgments Dr. Marta Guerra and Dr. Sean Shadomy for their guidance on this paper.

Author’s Affiliation: Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859

Correspondence to: William A. Londeree MD; Tripler Army Medical Center, Honolulu, HI 96859; Email: [email protected] Lower Waikeakua Falls (Photo: William Harner MD)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 23 in Hawai‘i and the Pacific

Nathanial K. Copeland MD; Wyatt R. Palmer DO; Paul K. Bienfang PhD

Abstract ally it has been noted that more severe cases of CFP reported Ciguatera fish poisoning (CFP) is a caused by fish containing to the Hawai‘i Department of Health involve consumption of (CTX). The is produced by the spp. which are then eaten by fish; humans contract the illness when the head (brain) or organs of the fish and less severe cases tend eating either fish that have eaten the algae, or carnivorous fish that have to involve consumption of only the muscle. eaten those fish. CTX is an odorless, tasteless, and colorless The manifestations of CFP are predominantly gastrointestinal that blocks voltage-sensitive Na+ channels and accumulates in many tissues and neurological, but also include other rare but potentially of the fish, especially the viscera. The illness is typically mild to moderate dangerous effects.1,2 Effects typically begin within a window in severity with gastrointestinal (diarrhea, cramping, nausea, vomiting) and of <1 to 48 hours from ingestion, with gastrointestinal symp- neurological (paraesthesias, cold , fatigue, pruritis) manifestations. toms occurring typically within 12 hours and neurological Rarely, the disease can be more severe with significant neuropathic or cardiac 2 effects such as and hypotension. Endemic to Hawai‘i and islands symptoms developing over the first 24 hours. Gastrointestinal throughout the Caribbean and Pacific, CFP incidence rates range from several effects include diarrhea, abdominal pain, nausea, and vomit- to thousands of cases per 100,000 per year. Since fishing is important for ing. These have the potential for significant dehydration, but local food supply, exportation, and recreation throughout the Pacific, CFP is are typically short-lived. Neurological effects include perioral medically and economically significant in these areas. We present a case of and stocking-glove distribution paraesthesias, myalgias, numb- CFP from Hawai‘i to illustrate the disease, demonstrating that the diagnosis is ness, cold allodynia (burning pain caused by exposure to cold primarily clinical, with confirmatory tests from fish samples available in some temperature), fatigue, pruritis, and rarely coma.1,2 Neurological cases. Treatment is supportive and symptomatic with no disease specific remedy. The prognosis for most cases is good with a short duration of self- symptoms can be variable in course, with most resolving in days limited symptoms, but for some cases neurological sequelae can become to weeks, though some can persist for years and are reported chronic. With no effective treatment, education on which species of reef fish to recur with exposure to non-CTX containing triggers (such and which body parts to avoid eating is essential in the prevention of CFP. as consumption of chicken or alcohol).2 Rare but significant cardiovascular effects do occur, including bradycardia and Introduction hypotension.1 Typically moderate, CFP can rarely result in Ciguatera fish poisoning (CFP) is a foodborne illness contracted death. by humans eating reef fish containing ciguatoxin (CTX) and is An endemic problem in Hawai‘i and many of the Pacific characterized predominantly by gastrointestinal and neurologi- Islands,3,4 cases of CFP are reported to the Hawai‘i Department cal manifestations. It is the most common marine poisoning of Health, with a total of 3 to 69 cases per year in the state, in the world1,2 and is a significant public health concern in the averaging 28.5 total cases per year from 2002-2011.4 With Caribbean, Hawai‘i, and the Pacific islands.3,4 underreporting of milder cases, it is likely that the actual local The CTX toxin is produced by the microalgae Gambierdiscus incidence is anywhere from 10 to 20 times higher than reported. spp., which are ingested by herbivorous reef fish that are then There have been two reported deaths from CFP in Hawai‘i eaten by larger carnivorous reef fish and serve as the primary occurring in 1964 after eating broiled reef fish including their source for human illness.1,2 The are soluble and viscera.8 There is a broad range of incidence across the Pacific bioaccumulate in greater concentrations as they move up the islands, with Samoa at about 1.6 cases per 100,000 per year and , making the larger carnivorous fish more likely to the Cook Islands at nearly 1,500 cases per 100,000 per year.3 cause harm to humans.5 However, consumption of any fish Fish are an important natural resource throughout the Pacific in the food chain can cause disease.1 The toxin is and fishing is a very common means of subsistence, putting colorless, odorless, and tasteless and is not affected by any many people at risk for CFP. Reef fishing also represents a food storage or preparation techniques.6 It is the one of the common sport in Hawai‘i, endangering both visitors and the most potent Na+ channel toxins known in mammals, causing local population. Based on data from the Hawai‘i Department activation of voltage-sensitive Na+ channels at very small (<1 of Health, the five most common fish associated with cases part per billion) concentrations, leading to its multiple clinical of CFP in the state from 1963 to 2012 are jack (ulua, kahala, manifestations as discussed below.2 Reef fish in particular are or papio), surgeon fish kole( ), (roi or hapu‘u), snap- associated with CFP, as these are the fish involved in the food pers (lehi, onaga, taape, or waha-nui), and wrasses (Figure 1; chain of the Gambierdiscus spp. Reef fish commonly associated Hawai‘i State Department of Health, unpublished data, Oct with CTX are many but include: barracudas, groupers, jacks, 2013). There are many local myths about how to determine moray eels, snappers, parrotfish, and surgeonfish.2,6,7 Due to which fish are safe, including avoiding fish from the leeward its lipid , CTX accumulates more heavily in several side of the island. From 2008 to 2012 researchers from the Uni- places in fish including the brain, liver, and gonads. Anecdot- versity of Hawai‘i cooperated with local fishermen to conduct

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 24 surveillance studies of roi caught across the state of Hawai‘i, confirmed CFP after consuming a reef fish caught in Hawai‘i.11 testing the fish for the presence of CTX. The map in Figure 2 The man and his wife both consumed a knifejaw fish that the represents the cumulative data from the island of O‘ahu.9 The man had caught while spear fishing in a reef off Kaua‘i. Both he study shows that no coast of any Hawaiian Island is free from and his wife had onset of typical ciguatera symptoms, including CTX-positive fish and it is speculated that any relationship to gastrointestinal upset and paraesthesias, within a few hours of the leeward side of an island is more likely due to which coast consuming the fish. His wife’s case was relatively mild and is more commonly fished rather than the presence or absence short in duration, but he progressed to develop more severe of CTX positive fish.10 neurological manifestations including severe neuropathy. He was unable to walk, speak, or feed himself and was hospitalized Example Case for more than 2 months. Remnants of the fish that the patient In 2009 the Honolulu Advertiser reported a case of a previ- ate were tested by the Department of Health and found to be ously healthy 53-year-old man who developed a severe case of positive for CTX.

Figure 1. Ciguatera incidents by type of fish consumed, Hawai‘i (1963-2012) (image courtesy Hawai‘i State Department of Health)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 25 Figure 2. Percent of groupers (roi) positive for CTX on the coasts of O‘ahu (image courtesy of Dr. P.K. Bienfang)

Discussion including neuropathy, fatigue, or pruritis chronically. There is A diagnosis of CFP is clinically based on the presence of typi- also evidence of sensitization, with affected individuals having cal gastrointestinal and neurological symptoms and history of more rapid onset of symptoms upon subsequent exposure to ingestion of a likely CTX containing fish. There are currently the toxin.2 no blood tests available to confirm poisoning with CTX.1,2 With no specific treatment available for CFP, prevention is a The current gold standard for confirming the diagnosis is the key component to the management of this disease, especially in testing of fish remnants for CTX (when they are available), as endemic areas such as Hawai‘i and the Pacific islands. The most illustrated in the case above.1 Treatment of CFP is supportive, effective approach to preventing CFP is to avoid reef fish which with symptomatic treatment of gastrointestinal manifestations are more likely to contain CTX. Fish containing CTX cannot and supportive care in more severe cases with bradycardia and be reliably distinguished from safe fish based on appearance, hypotension.2 There are no proven treatments for neurological taste, or smell. Some traditional methods exist in Hawai‘i and manifestations. has shown promise in ameliorating the the Pacific Islands for determining which fish may be at risk neurological sequelae, but the only double-blind, randomized for causing ciguatera, including feeding it first to the family pet controlled trial to date showed no difference when compared to or the oldest member of the family, or avoiding fish that flies normal saline and highlighted concerns for hypotension caused avoid, but these methods cannot be recommended as they are by mannitol.2,6 Some limited data suggest that neuromodulat- neither safe nor reliable. There is a common belief that people ing medications such as may be beneficial, but should avoid larger individual fish of a given species, but any controlled trials are lacking.2 While no specific remedies are size of fish can potentially harbor sufficient amounts of CTX to available in austere environments to prevent or treat CFP, there elicit symptoms.10 In the past commercially-produced, portable are many local remedies throughout the Pacific Islands such as CTX detection kits were available to test fish prior to eating, plant extracts that are unproven by research.1,7 One common but their production has been discontinued due to a significant traditional remedy employed stems from the tree heliotrope, number of false negative tests.12 People should avoid consump- which is found in Hawai‘i and throughout the Pacific Islands; tion of the liver, brain, or gonads of reef fish, as these tissues no studies confirming its efficacy have been published. sequester much higher levels of CTX than the muscle tissue. Most cases do not cause long term effects; however, there are The key to prevention is educating the populace about the risks some patients that will have persistent neurological symptoms, of eating reef fish in endemic areas. In cases where this is not

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 26 feasible, such as in areas where reef fish are a primary source Authors’ Affiliation: Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 of subsistence, education about avoiding consumption of the viscera (which have a higher concentration of the toxin) is also Correspondence to: important. Nathanial K. Copeland MD; 1 Jarrett White Rd, Honolulu, HI 96859; Ph: (808) 433-1377; Email: [email protected] Conclusion References Ciguatera fish poisoning is an important fish-borne disease in 1. Dickey RW, Plakas SM. Ciguatera: A public health perspective. Toxicon. 2010;56(2):123-136. doi:10.1016 /j.toxicon.2009.09.008. Hawai‘i and the Pacific islands. Though most cases have mild 2. Isbister GK, Kiernan MC. Neurotoxic marine poisoning. Lancet Neurol. 2005;4(4):219-228. to moderate gastrointestinal and neurological symptoms, the 3. Skinner MP, Brewer TD, Johnston R, Fleming LE, Lewis RJ. Ciguatera fish poisoning in the Pacific islands (1998 to 2008). PLoS Negl Trop Dis. 2011;5(12):e1416. doi:10.1371/journal. potential for more severe and even life-threatening illness ex- pntd.0001416 ists. There is significant variation in the incidence of the disease 4. State of Hawaii Department of Health. 10-Year Summary of Reported Cases of Notifiable Diseases Hawai’i 2002-2011. http://hawaii.gov/health/about/about/pr/New%20Disease%20 depending on location and it is important for travelers to these Template%20for%20WEB%20publish2002_2011.html. Accessed September 3, 2013. areas to be familiar with the local risk of CFP and to make deci- 5. Bienfang PK, Trapido-Rosenthal H, Lows EA. Magnification of risks: /bio- magnifications in food chains. In: Meyers RA, ed.Encyclopedia of Sustainability Science and sions about eating reef fish accordingly. Diagnosis is clinical, Technology. New York, NY: Springer; 2012. with confirmatory fish tissue sampling. Treatment is supportive 6. Centers for Disease Control and Prevention. Ciguatera fish poisoning--New York City, 2010- 2011. MMWR Morb Mortal Wkly Rep. 2013;62(4):61-65. and symptomatic with no disease-specific remedy proven. Due 7. Bienfang PK, Parsons ML, Bidigare RR, Laws EA, Moeller PDR. Ciguatera fish poisoning: to the lack of treatment options, prevention via avoidance of A synopsis from ecology to toxicity. In: Walsh PJ, Smith SL, Fleming LE, Solo-Gabriele HM, Gerwick WH, eds. Oceans and Human Health: Risks and Remedies from the Sea. New York, likely CTX containing fish is essential, or at a very minimum NY: Elsevier Science Publishers; 2008:257-270. avoiding the head and viscera of reef fish. 8. Anderson BS, Sims JK, Wiebenga NH, Sugi M. The epidemiology of ciguatera fish poisoning in Hawaii, 1975-1981. Hawaii Med J. 1983;42(10):326-334. 9. Oahu roi results. Dr. P.K. Bienfang’s website on ciguatera testing in roi (peacock groupers). Disclosures http://www.fish4science.com/Oahu_map_of_Roi.html. Accessed September 3, 2013. 10. Bienfang P, DeFelice S, Laws E, Wallsgrove N, Caldwell P. Ciguatoxicity in the main Hawaiian The authors report no financial conflicts of interest. Islands: special and temporal variability in the introduced reef Cephalopholis argus. J Res Environ Sci Toxicol. 2012;1(4):47-57. Disclaimer 11. Diana L. Isle man’s case shows ciguatera’s risk. Honolulu Advertiser. http://the.honoluluadvertiser. com/article/2009/Nov/09/ln/hawaii911090324.html. Accessed September 3, 2013. The views expressed in the manuscript are those of the authors 12. Bienfang P, DeFelice S, Dowling A. Quantitative evaluation of commercially available test kit for and do not reflect the official policy or position of the Depart- ciguatera in fish.Food and Nutrition Sciences. 2011;2(6):594-598. doi:10.4236/fns.2011.26083. ment of the Army, Department of Defense or United States Government.

Acknowledgment The authors would like to thank the Hawai‘i Department of Health’s Disease Investigation Branch for providing data on the incidence of ciguatera by type of fish consumed and the graph used in Figure 1.

Peacock (Cephalopholis argus) [Photo: Russell Gilbert MD]

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 27 The Potential Danger of Eating Wild Lettuce: A Brief Review of Human Rat Lungworm Infection

Evan C. Ewers MD and Sarah K. Anisowicz MD

Abstract of A. cantonensis include the rat species of Rattus norvegicus, Angiostrongylus cantonensis, the causative agent of human rat lungworm R. rattus, and R. exulans, which acquire the infection through disease, is the most common cause of eosinophilic meningitis worldwide and ingestion of third-stage (L3) larvae by eating a slug or snail. is endemic throughout Asia Pacific. It is acquired through the consumption of infected freshwater mollusks or contaminated produce. Human angiostrongyli- Ingested worms travel from the rat’s gut to the bloodstream, asis is usually a self-limited disease presenting with headache and various eventually making their way to the central . In neurologic sequelae varying from cranial nerve palsies to radiculitis and/or the brain, they develop into the fifth stage (L5) young adults, paresthesias. Fatal cases are rare, and manifest as fulminant meningomy- and travel via the cerebral venous system and make their way eloencephalitis. The diagnosis is made through the use of clinical history, to the pulmonary arteries, where the females lay eggs. The exam, and laboratory data including peripheral blood counts, cerebrospinal eggs make their way to the distal lung, where they hatch into fluid (CSF) examinations, and serologic or molecular diagnostic techniques. first-stage larve (L1), extravasate, and migrate up the trachea Medical therapy is largely focused on symptomatic relief, and includes an- algesics, lumbar puncture, and corticosteroids. In resource-limited settings, where they are swallowed and excreted in the rat’s feces. Once prevention is key, and the use of analgesics can provide symptomatic relief in the environment, the L1 larvae mature into L3 larvae, and after infection. Efforts to increase disease awareness have been made in are ingested by a snail, slug, or other intermediate or paratenic endemic areas, as evidenced by the recent Rat Lungworm Disease Scien- host.5 If the snail or slug is consumed by a rat, the life cycle tific Workshop which was held in Honolulu in 2011. The proceedings of the is repeated. However, the infection of accidental hosts, such workshop were published in a supplement to this journal (Hawaii J Med Public as species of crustaceans, frogs, monitor lizards, and planaria Health. Jun 2013;72(6):Supp 2). However, wilderness medicine and travel results in larvae remaining in the L3 stage inside that animal, medicine specialists must also be aware of the disease, how it is contracted, its presentation, and treatment options should they encounter a patient who which makes them capable of infection once consumed by is in or has returned from an endemic area. This brief review highlights eo- rats, humans, or other mammals. If consumed by a human, the sinophilic meningitis caused by A. cantonensis, including an example case, larvae make their way to the CNS, but are unable to adequately an overview of its clinical presentation, treatment options, and prevention. mature to complete their life cycle. Human infection with rat lungworm results from the ingestion Background of either infected snails, prawns, crabs or contaminated fruits and The parasitic nematode Angiostrongylus cantonensis is the vegetables. Since it was first identified as a human pathogen in causative agent of rat lungworm disease, and the most common 1944, a number of outbreaks of eosinophlic meningitis occurring identified cause of eosinophilic meningitis worldwide. Although in China, Taiwan, Japan, Southeast Asia, Australia, Hawai‘i, first isolated from the pulmonary artery of a rat by Chen in 1935, and the South Pacific have been attributed to A. cantonensis, it was not identified as a human pathogen until it was isolated and cases have been identified on the six inhabited continents.2 from a case of eosinophilic meningitis in Taiwan ten years Although the increasing identification of clinical cases is likely later.1 Approximately 2900 cases of eosinophilic meningitis multifactorial, it is widely accepted that international com- have been reported in the literature since 1944 as a result of merce and shipping have contributed to the nematode’s spread rat lungworm infection, although it is believed this number is through the transportation of either infected rats, snails, slugs, largely underreported, as many infections may be subclinical or or other hosts. Recently, A. cantonensis has been found to be occur in areas where specific diagnostic testing is not routinely the etiologic agent of eosinophilic meningitis in a number of performed.2 Today, rat lungworm is considered endemic in most travelers returning to northern climates from endemic areas. 6 parts of the Asia-Pacific region, and new cases are now routinely This has highlighted the importance of proper education and being identified in previously non-endemic areas. increased awareness of both travelers and physicians. Travelers Much is unknown about specific pathogenic mechanisms who enjoy camping, consuming wild foodstuffs, or sampling involved in human rat lungworm infection producing clinical local or cultural cuisine in endemic areas should be aware of disease, but the biology and life cycle of A. cantonensis are the potential risks, and how to mitigate them. well described in the scientific literature.2-5 Angiostrongylus cantonensis is a member of the family Angiostrongylidae in the Relevance to Hawai‘i and Asia Pacific superfamily Metastrongyloidae, of which only 20 species in the Angiostrongylus cantonensis has been well-established as a genus Angiostrongylus are known. Of these, two species—A. causative agent of eosinophilic meningitis in Hawai‘i since cantonensis and A. costaricensis—cause disease in humans, 1960, although it did not become a reportable disease in the although the latter is only associated with a gastrointestinal illness state of Hawai‘i until 2007.7,8 Hochberg, et al, identified 24 most prevalent in Central and South America. The definitive hosts cases of eosinophilic meningitis caused by A. cantonensis in

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 28 Figure 1. Life-cycle of Angiostrongylus cantonensis. Life cycle obtained from http://www.cdc.gov/parasites/angiostrongylus/biology.html. Accessed 15 December 2013.

Hawai‘i between 2001-2005, with cases reported in the islands since the early 1960s, with cases reported in French , of O‘ahu, Maui, Lana‘i, and the island of Hawai‘i, which had Samoa, and the Marshall Islands between 1961 and 1964.7,14,15 the highest incidence.9 Since 2007, 33 cases of eosinophilic Numerous outbreaks have occurred in Asia, particularly in meningitis due to A. cantonensis have been reported in the the northeastern provinces of Thailand, and throughout inland state. 8 In many of these cases, patients have consumed either China and Taiwan, where cases are still routinely documented. contaminated vegetables or snail species acting as intermediate Of the nearly 2900 cases that have been reported in the medical hosts. In Hawai‘i, several species of snails have been identified literature, approximately 75% have been reported from Thai- as carriers of the rat lungworm nematode, including the giant land and China.2 Many cases in these regions result from the African snail Achatina fulica, and the relatively new, invasive consumption of raw snails in cultural dishes, or consumption semi-slug Paramarion martensi, which is now abundant through- of contaminated raw vegetables or their juices.16-19 For visitors, out the Hawaiian archipelago.10-12 Environmental evaluation it is important to be mindful that in certain areas eating local of mollusk species on the islands of O‘ahu and Hawai‘i have cuisine can result in serious illness. This should also serve as demonstrated infection rates ranging from 24-88% depending a reminder to travel medicine specialists to discuss potential on species and location.12,13 risks with patients traveling to these areas, particularly if they A. cantonensis has also been identified as the causative are planning on camping, or immersing themselves in local agent of eosinophilic meningitis throughout the South Pacific culture.

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 29 Example Case the majority of patients developing symptoms by two weeks A seven-year-old previously healthy boy re-presented to a following the inciting event.18 However, incubation periods as pediatric clinic with his mother for headache, vomiting, and short as one day have been reported. 20 fatigue. The patient was in his usual state of health until eight The manifestations of the infection are primarily localized days earlier, when he complained of a headache which improved to the , where it is known to cause following administration of acetaminophen. The mother noted mild, subacute, or fulminant eosinophilic meningitis. Rarely, that the patient seemed more fatigued, preferring to watch tele- ocular manifestations can occur with nematode invasion in the vision instead of playing with his older siblings. Seven days 3 major chambers of the eye.21 The most common presenting earlier he began to have intermittent, non-bloody, non-bilious symptoms of human angiostrongyliasis and various clinical vomiting. Five days prior he was evaluated in the clinic for manifestations have been well-described in case reports, series, headaches and vomiting, and diagnosed with . and epidemiologic studies on the disease.2,6,18,19,22,23 Headache His mother was instructed to encourage increased fluid intake, is the most common early symptom and often the presenting and return should his symptoms not resolve. At the time of re- complaint, typically occurring in greater than 90% of those af- presentation, the mother denied any fevers, rashes, diarrhea, or flicted. Headache, as well as nausea and vomiting, is attributed upper respiratory symptoms. primarily to increased intracranial pressure, or direct neuronal On exam, the patient was a non-toxic appearing male who damage caused by both dying larvae and the host immune re- was alert, although slightly irritable. Vital signs included tem- sponse. In some cases, serial lumbar punctures have resulted in perature of 38.6 C, blood pressure of 104/64, 98, and symptomatic decrease of a patient’s headache, although these respiratory rate of 22. Mucous membranes were dry. The patient have not been associated with curing infection.24,25 Subjective was protective of his neck and would not voluntarily move it. neck pain and stiffness, fatigue, fever, visual complaints, and Passive range of motion of the neck was made difficult by pa- paresthesias develop between 30%-50% of patients, occurring tient non-compliance with exam. The patient was admitted for in the early course of the disease. The paresthesias experienced mild dehydration and concern for meningitis. Complete blood are often profound, and range from burning and tingling, to count showed a leukocytosis of 14,000, hemoglobin of 14.3 g/ symptoms reflective of an acute painful radiculitis with hyperes- dl, hematocrit of 41%, and platelets of 420,000. Leukocyte dif- thesia. Neurologic symptoms and signs can also result in cranial ferential was notable for eosinophilia of 18%. Lumbar puncture nerve palsies, and rarely, altered sensorium. Upper respiratory was unremarkable with protein of 60 mg/dL, of 70 mg/ symptoms including sinus congestion, rhinorrhea, sore throat, dL, no red blood cells and few eosinophils without organisms and dry cough can be seen early in the disease course. In ocular on gram stain. Notably, the patient had decreased complaint of cases, the presenting complaint is usually blurred vision develop- headache after the procedure. On day 2 of admission, patient ing over several weeks. Overall, the clinical presentation of A. complained of worsening headache, and a repeat lumbar punc- cantonensis varies broadly, and can include mild self-resolving ture resulted in symptomatic relief of the patient’s headache. symptoms to fulminant meningomyeloencephalitis resulting in Test performed on CSF were negative for enterovirus, herpes coma and permanent neurologic deficits. Death has been reported simplex virus, syphilis, and bacterial organisms. in only a few cases.20,25 These catastrophic cases are associated Further history taken during admission revealed he ingested with heavy infections found to have large nematode burden a snail from the family garden after being “dared” by his older and advanced inflammatory reaction involving macrophages, brothers three days before the onset of symptoms. Based on T-cells, eosinophils, and neutrophils on pathologic review. this history and continued peripheral eosinophilia throughout Physical findings are related to the onset of neurologic sequelae admission, he was diagnosed with eosinophilic meningitis. At the and can include decreased , bowel or bladder dysfunc- time of discharge, the patient continued to complain of headache tion, muscle weakness, cranial nerve deficits, and evidence of which was controlled with oral ibuprofen and acetaminophen. increased intracranial pressure. Non-suppurative pharyngitis He was followed closely by his outpatient provider and did not and cervical adenopathy have been reported. Meningeal signs develop any further neurologic symptoms with resolution of are inconsistently reported in association with eosinophilic headache by one month after admission. meningitis.18 In cases of ocular angiostrongyliasis, living larvae can be observed in the anterior, vitreal, or retinal chambers, with Clinical Discussion accompanied findings of epithelial alteration and subretinal As in this example case above, ingestion of larvae occurs either tracking.21 by direct consumption of contaminated mollusk species, or Diagnosis of rat lungworm infection is often difficult to es- through the ingestion of contaminated produce. In Hawai‘i, both tablish. Typically, a combination of patient history, symptoms, kinds of exposures have been reported in the clinical literature, clinical findings, and laboratory tests are required to make the and similar exposures resulting in outbreaks in Thailand, China, diagnosis. The “gold” standard is isolation of the nematode and the South Pacific. Incubation periods typically last from from the CSF, occurring in only 2-12% of cases.18,25 However, 5-40 days post exposure. In a study of eosinophilic meningitis it should be noted that nematode isolation from CSF is more in Thailand, 83% of patients reported symptom onset by 20 common in pediatric patients than in adults. Absolute peripheral days following ingestion of a raw freshwater mollusks, with eosinophilia (> 450/µL) as seen on CBC, particularly in the

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 30 setting of leukocytosis, and the presence of eosinophils in CSF traditional Thai “Koi-Hoi” marinade consisting of spices and are frequently seen in human infections. Chemical examina- citrus juice resulted in decreased larval infectivity, particularly tion of CSF also demonstrates elevated protein, and normal to when a local 80-proof spirit was added.17 In their study, an slightly decreased glucose.18-20,22-26 Serologic studies can also be 80% decrease in motile larvae was seen after 60 minutes in employed in the diagnosis. Tsai, et al, reported the presence of the marinade alone, or 5 minutes in the marinade followed by anti-Angiostrongylus antibodies in the serum in 100% of patients 30 minutes in the alcohol drink. A 100% non-motile rate was as well as in the CSF of 80% of patients, indicating that even seen when the snails were allowed to marinate for 25 minutes during acute infection serologic testing plays an important role followed by soaking in alcohol for 30 minutes. This serves to in assisting with diagnosis. 19 Recently, gene amplification using demonstrate that household products, or those available to camp- polymerase chain reaction has been employed to identify the ers and hikers can be used to reduce risk. The use of vinegar, presence of nematodes in both serum and CSF. 24 As molecular salt solution, and 1.5% bleach solution have also been shown and point-of-care diagnostic techniques for parasitic diseases to decrease larval infectivity in A. costaricensis after soaking improve in the coming years, rapid definitive diagnosis using contaminated produce in the for 15 minutes.29 To our CSF samples might become possible, and have great utilization knowledge, this study has not been replicated for A. cantonen- in endemic areas. sis, and might be a direction for future research as cases of the Since the 1990s, advances in neuroradiology has also played disease are spreading globally and awareness is increasing. a role in assisting with diagnosis of eosinophilic meningitis. Hyperintense areas in white matter seen on T2-weighted images Treatment in Non-Austere Environments have been observed in patients with human angiostrongyliasis, Clinical variability is broad and symptoms often guide medical as well as post-gadolinium enhancement of subcortical white intervention. Mild cases resolve spontaneously, requiring only matter and affected cranial nerves on T1-weighted images. symptomatic therapy. For highly symptomatic cases, serial Leptomeningeal enhancement is also frequently seen.22,24,27 lumbar punctures have been demonstrated to provide symp- Interestingly, Tsai and colleagues observed a significant cor- tomatic relief for headache, nausea, and vomiting caused by relation (P < .05) between T1 signaling on MRI and clinically increased intracranial pressure.18,22,24-26 Antihelmintic therapy is more severe headache, as well as CSF and peripheral eosino- controversial due to the theoretical risk that immune reaction philia. To date, there has been no associated pathognomonic caused by rapidly dying worms can exacerbate patient’s neu- radiographic finding in patients with eosinophilic meningitis. rologic symptoms and lead to potentially catastrophic results. However, neuroradiology can be used to support the diagnosis However, case-series and epidemiologic studies published and rule out other potential causes—amebiasis, neurocysticer- in which antihelmintic therapy was used have not reported cosis, gnathostomiasis, and paragonamiasis, among others. significant adverse reactions directly related to their use, and most of the treated patients have made full recovery.15,19,20 The Treatment in Resource-Constrained role of corticosteroids has also been evaluated in the treatment Environments of eosinophilic meningitis, particularly with the goal of reduc- Campers, hikers, farmers, and adventurous eaters are among ing cerebral inflammation caused by the immune response. In those individuals who should be educated regarding the risks of most situations, corticosteroids have not been shown to shorten human angiostrongyliasis, including its mechanism of infection disease course.2,18,19 However, Chotmongkol, et al, reported in a and the disease sequelae. Luckily, the vast majority of reported randomized, controlled trial that two weeks of corticosteroids cases have occurred within some proximity to medical atten- decreased headache duration when compared with placebo, as tion. The best way to manage eosinophilic meningitis is to limit well as decreasing repeat lumbar punctures in the experimental exposure. This is accomplished by avoiding the consumption of group.30 Additionally, the same author demonstrated their safety raw freshwater mollusks including snails, slugs, prawns, crab, for use in patients with eosinophilic meningitis.31 Corticosteroids and even raw freshwater fish. This includes washing fresh fruits have also been evaluated when used concurrently with antihel- and vegetables, particularly lettuces, and ensuring that roadside mintics such as albendazole. In their study, Chotmongkol, et al, juice stands are serving products made from properly washed found that adding albendazole to the corticosteroid regimen did and peeled produce. not result in shortened disease course or improved symptomatic Since snails and their slime can be found in and on fresh relief when compared with steroids alone.32 Importantly, no fruits and vegetables, washing the produce prior to consump- adverse drug outcomes were reported in their study for either tion is an important step in the food preparation process. A the control or treatment groups. comparison of salt, bleach, and vinegar solutions demonstrated Based on the available evidence, there are no current official no significant difference compared with tap water alone when recommendations regarding treatment of eosinophilic meningitis used to remove snails/slugs from produce, although multiple caused by A. cantonensis. Generally, it is accepted that the use washing/rinsing cycles was found to decrease snail burden.28 of corticosteroids (prednisolone at 20mg three times daily for However, the use of different household chemicals and treat- 14 days) might provide some benefit in symptomatic reduction, ments has been shown to decrease larval infectivity in rats. with minimal adverse effects. The use of albendazole or another Eamsobhana, et al, reported that mixing raw snails in the antihelmintic agent remains controversial due to theoretical

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 31 6. Slom TJ, Cortese MM, Gerber SI, et al. An outbreak of eosinophilic meningitis caused by risks, although these have not been demonstrated in limited Angiostrongylus cantonensis in travelers returning from the Caribbean. N Engl J Med. Feb clinical studies. However, their use is usually not required and 2002;346(9):668-675. 7. Rosen L, Chappell R, Laqueur GL, Wallace GD, Weinstein PP. Eosinophilic meningoencephalitis should be reserved for case non responsive to symptomatic caused by a metastrongylid lung-worm of rats. JAMA. Feb 24 1962;179:620-624. management, or those with severe systemic effects. 8. Health HDo. Ten-year Summary of Reported Cases of Notifiable Disease, Hawaii 2003-2012. 2013; http://health.hawaii.gov/docd/files/2013/07/dib_disease_counts_rates.pdf. Accessed December 15, 2013. Conclusion 9. Hochberg NS, Park SY, Blackburn BG, et al. Distribution of eosinophilic meningitis cases attribut- Angiostrongylus cantonensis able to Angiostrongylus cantonensis, Hawaii. Emerg Infect Dis. Nov 2007;13(11):1675-1680. is the most common cause of 10. Hollingsworth RG, Howe K, Jarvi SI. Control measures for slug and snail hosts of Angiostrongylus eosinophilic meningitis worldwide, and is endemic throughout cantonensis, with special reference to the semi-slug Parmarion martensi. Hawaii J Med Public Health. Jun 2013;72(6 Suppl 2):75-80. the Asia-Pacific region. It has been shown to cause disease in 11. Hollingsworth RG, Kaneta R, Sullivan JJ, et al. Distribution of Paramarion cf. martensi (Pulmo- returning travelers. Travelers to endemic areas, particularly those nata: Helicarionidae), a New Semi-Slug Pest on Hawai’i Island, and Its Potential as a Vector for Human Angiostrongyliasis. Pacific Science. 2007;61(4):457-467. who camp, eat local cultural cuisine, consume raw freshwater 12. Qvarnstrom Y, Bishop HS, da Silva AJ. Detection of rat lungworm in intermediate, definitive, mollusks, or eat raw fruits and vegetables are at risk of acquiring and paratenic hosts obtained from environmental sources. Hawaii J Med Public Health. Jun 2013;72(6 Suppl 2):63-69. the nematode infection. Human angiostrongyliasis has a variable 13. Kim JR, Hayes KA, Yeung NW, Cowie RH. Definitive, intermediate, paratenic, and accidental clinical presentation that can range from a short, self-limited hosts of Angiostrongylus cantonensis and its molluscan intermediate hosts in Hawa’i. Hawaii J Med Public Health. Jun 2013;72(6 Suppl 2):10. illness, to fulminant meningoradiculomyelitis, or encephalitis, 14. Rosen L, Laigret J, Bories S. Observations on an outbreak of eosinophilic meningitis on Tahiti, with permanent neurologic sequelae and death. The mainstay French Polynesia. Am J Hyg. Jul 1961;74:26-42. 15. Rosen L, Loison G, Laigret J, Wallace GD. Studies on eosinophilic meningitis. 3. Epidemiologic of treatment includes management of headache through LP, and clinical observations on Pacific islands and the possible etiologic role of Angiostrongylus analgesics, and potentially steroids or antihelminthic agents, cantonensis. Am J Epidemiol. Jan 1967;85(1):17-44. 16. Eamsobhana P. Angiostrongyliasis in Thailand: epidemiology and laboratory investigations. although the role of the latter is controversial. Hawaii J Med Public Health. Jun 2013;72(6 Suppl 2):28-32. 17. Eamsobhana P, Yoolek A, Punthuprapasa P, Yong HS. Thai koi-hoi snail dish and angiostron- Disclosures gyliasis due to Angiostrongylus cantonensis: Effects of food flavoring and on the third-stage larvae in infected snail meat. Foodborne Pathog Dis. Apr 2009;6(3):401-405. The authors reported no conflicts of interest. 18. Punyagupta S, Juttijudata P, Bunnag T. Eosinophilic meningitis in Thailand. Clinical studies of 484 typical cases probably caused by Angiostrongylus cantonensis. Am J Trop Med Hyg. Nov 1975;24(6 Pt 1):921-931. Disclaimer 19. Tsai HC, Lee SS, Huang CK, Yen CM, Chen ER, Liu YC. Outbreak of eosinophilic meningitis associated with drinking raw vegetable juice in southern Taiwan. Am J Trop Med Hyg. Aug The views expressed in this abstract/manuscript are those of 2004;71(2):222-226. the author(s) and do not reflect the official policy or position 20. Kliks MM, Kroenke K, Hardman JM. Eosinophilic radiculomyeloencephalitis: an angiostrongyli- asis outbreak in American Samoa related to ingestion of Achatina fulica snails. Am J Trop Med of the Department of the Army, Department of Defense, or the Hyg. Nov 1982;31(6):1114-1122. US Government. 21. Sinawat S, Sanguansak T, Angkawinijwong T, Ratanapakorn T, Intapan PM, Yospaiboon Y. Ocular angiostrongyliasis: clinical study of three cases. Eye (Lond). Nov 2008;22(11):1446-1448. 22. Hochberg NS, Blackburn BG, Park SY, Sejvar JJ, Effler PV, Herwaldt BL. Eosinophilic meningitis Acknowledgements attributable to Angiostrongylus cantonensis infection in Hawaii: clinical characteristics and The authors would like to thank the Editors of the Wilderness Medicine potential exposures. Am J Trop Med Hyg. Oct 2011;85(4):685-690. Supplement for considering our article. We also wish to thank the library 23. Tsai HC, Liu YC, Kunin CM, et al. Eosinophilic meningitis caused by Angiostrongylus cantonensis: report of 17 cases. Am J Med. Aug 2001;111(2):109-114. staff at Tripler Army Medical Center for assisting with the literature review, 24. Kwon E, Ferguson TM, Park SY, et al. A severe case of Angiostrongylus eosinophilic meningitis as well as our reviewers for providing insightful comments and suggestions. with encephalitis and neurologic sequelae in Hawa’i. Hawaii J Med Public Health. Jun 2013;72(6 Suppl 2):41-45. Authors’ Affiliation: 25. Yii CY. Clinical observations on eosinophilic meningitis and meningoencephalitis caused by Angiostrongylus cantonensis on Taiwan. Am J Trop Med Hyg. Mar 1976;25(2):233-249. Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 26. Thyssen A, Mitchell M, Qvarnstrom Y, Rao S, Benke TA, Glode MP. Eosinophilic meningitis in a previously healthy 13-year-old child. Pediatr Infect Dis J. Feb 2013;32(2):194, 198. Correspondence to: 27. Tsai HC, Liu YC, Kunin CM, et al. Eosinophilic meningitis caused by Angiostrongylus cantonensis Evan C. Ewers MD; Department of Medicine, Tripler Army Medical Center, Honolulu, associated with eating raw snails: correlation of brain magnetic resonance imaging scans with HI 96859; Ph: (808) 433-9772; Email: [email protected] clinical findings. Am J Trop Med Hyg. Mar 2003;68(3):281-285. 28. Yeung NW, Hayes KA, Cowie RH. Effects of washing produce contaminated with the snail and slug hosts of Angiostrongylus cantonensis with three common household solutions. Hawaii J References Med Public Health. Jun 2013;72(6 Suppl 2):83-86. 1. Chen HT. A new pulmonary nematode of rats, Pulmonema cantonensis ng, nsp from Canton. 29. Zanini GM, Graeff-Teixeira C. Inactivation of infective larvae of Angiostrongylus costaricensis Annals of Parasitology. 1935;13:312-317. with short time incubations in 1.5% bleach solution, vinegar or saturated salt solution. 2. Wang QP, Lai DH, Zhu XQ, Chen XG, Lun ZR. Human angiostrongyliasis. Lancet Infect Dis. Acta Trop. Jan 2001;78(1):17-21. Oct 2008;8(10):621-630. 30. Chotmongkol V, Sawanyawisuth K, Thavornpitak Y. Corticosteroid treatment of eosinophilic 3. Cowie RH. Biology, systematics, life cycle, and distribution of Angiostrongylus cantonensis, meningitis. Clin Infect Dis. Sep 2000;31(3):660-662. the cause of rat lungworm disease. Hawaii J Med Public Health. Jun 2013;72(6 Suppl 2):6-9. 31. Chotmongkol V, Wongjitrat C, Sawadpanit K, Sawanyawisuth K. Treatment of eosinophilic 4. Kliks MM, Palumbo NE. Eosinophilic meningitis beyond the Pacific Basin: the global dispersal meningitis with a combination of albendazole and corticosteroid. The Southeast Asian journal of a peridomestic zoonosis caused by Angiostrongylus cantonensis, the nematode lungworm of tropical medicine and public health. Mar 2004;35(1):172-174. of rats. Soc Sci Med. Jan 1992;34(2):199-212. 32. Chotmongkol V, Kittimongkolma S, Niwattayakul K, Intapan PM, Thavornpitak Y. Comparison of 5. Mackerras MJS, D.F. The life-history of rat lungworm, Angiostrongylus cantonensis (Chen) prednisolone plus albendazole with prednisolone alone for treatment of patients with eosinophilic (Nematoda: Metastrongylidae). Australia Journal of Zoology. 1955;3:1-21. meningitis. Am J Trop Med Hyg. Sep 2009;81(3):443-445.

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 32 Heat Illness in Hawai‘i

Sarah Gordon MD

Abstract Heat illness is a commonly encountered health problem in the Hawaiian and radiation are no longer effective. Environmental conditions Islands. Year round warm , proximity to the equator, and high also affect evaporative cooling. A water vapor pressure gradient humidity combined with a plethora of opportunities for outdoor activities put must exist for sweat to evaporate and release energy into the many individuals at risk. This paper will focus on the physiology, identification, environment. In high humidity evaporation becomes ineffec- and treatment of varying forms of heat illness. Severe heat illness can be life tive for transferring heat (typically around relative humidity threatening. All outdoor enthusiasts should have a basic understanding of how to recognize this potentially life-threatening condition and employ preventive > 75%). Intrinsic factors that decrease ability to compensate measures. We will discuss appropriate management in pre-hospital and for generation of heat energy include age (both very young hospital settings. Early recognition and cooling are the most crucial aspects and very old individuals), stimulants, poor cardiovascular fit- of the management of heat illness. ness, and possibly the most modifiable risk factor, dehydration. Studies suggest that during intense exercise in the heat for Background every one percent of body mass lost from dehydration there is The human body’s temperature is regulated in the pre- a concomitant increase in core body temperature of 0.22° C.3 optic nucleus of the anterior , which in normal The human body also has significant adaptive cellular mecha- physiology is set at a core temperature of 98.6° F ± 2 degrees nisms in place to counteract heat illness. A highly conserved (37 C ± 1 degree). Outside of this range, the human body has response to physiologic stress including and hy- the ability to tolerate significantly colder temperatures, but at poxia exists in nearly all prokaryotic and eukaryotic cells. This warmer temperatures, particularly above 105° F, physiologic process is largely mediated by heat shock proteins. These are dysfunction occurs. transcriptionally inducible molecular chaperones. They work There are a variety of changes that occur on a cellular level to prevent the formation of damaged protein aggregates and in extreme heat. Elevated temperatures affect the exchange assist proteins in the acquisition of their native structures. It is of ions across transport membranes in all cells. This process, theorized that they are a physiologic response to cellular stress, coupled with alterations in renal blood flow, and changes in rather than a prophylactic process already in place. Studies have plasma volume, can lead to a variety of electrolyte derange- shown those with high basal levels of heat shock proteins are ments. Hyperthermia causes changes in the structure of cellular more likely to experience acute heat induced illness.2 These organelles including disruption of microfilaments and swelling proteins may represent a biomarker to assess susceptibility to of the mitochondria and the endoplasmic reticulum, leading heat stress. When these defenses are overwhelmed by either to collapse of the cytoskeleton and deformation of the plasma passive heat accumulation (classic heat stroke) or by generation membrane.1 Reaction kinetics dictate that rate increases with of excessive heat energy via activity (exertional heat stroke), heat, however, above a certain temperature reactions are unable heat illness occurs. to occur since the responsible enzyme begins to denature.2 To prevent heat illness, the body has cooling mechanisms to Relevance to Hawai‘i and Asia-Pacific remove heat. Evaporation, radiation, , and conduc- Heat illness on a wide spectrum is a common threat to people tion are the four main processes which reduce heat energy. who spend time outdoors in Hawai‘i. On all the islands, May Evaporation occurs when water vaporizes from the skin and through October is considered summer and winter the rest of respiratory tract. This is the body’s most effective mechanism the year. Honolulu is a well studied example of a sea level cli- for getting rid of heat (an example would be an athlete sweating mate, where summer highs average 85° F while winter highs in the hot sun). Radiation occurs when heat is directly emitted average 78° F. Due to proximity to the equator the UV index is into the environment. Convection is the transfer of heat to a almost always high, with an average index of 6-7 in the winter liquid overlying the body (eg, a swimmer cooling off in the and 11-12 for summer months. Recent research suggests that water). Conduction is direct transfer of heat to a cooler object temperatures will be increasing for the Hawaiian Islands in (eg, application of an ice pack).1 coming years. In Honolulu, Hawai‘i, the average temperature These processes all require a cardiovascular system that is has increased 4.4° F over the last century and research suggests able to increase blood flow to the distal vasculature to facilitate it will continue to increase, while precipitation has decreased transfer of heat from the body core to the skin, where the four approximately 20% over the last 90 years.4, 5 mechanisms for dissipating heat can take effect. During high Due to year round warm temperatures and sunshine, Hawai‘i heat loads, blood flow to the skin increases drastically to enable is a popular tourist destination. There are many outdoor activities these processes. However, when the ambient temperature is which require exertion, including hiking and water sports, both higher than the body’s core temperature, convection, conduction, of which result in prolonged sun exposure. Non-acclimatized or

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 33 poorly conditioned individuals, as well as young children and myocardial infarction is a potential concern, as are the elderly are particularly at risk of experiencing heat illness due to electrolyte derangements including massive potassium under these conditions. shifts. Other physiologic complications include , In addition, there are numerous organized sporting events. acute kidney injury from either decreased renal perfusion in A glance at a calendar for one of Honolulu’s sporting events the setting of massive hemodynamic compromise and/or pig- organizations shows an average of eight organized races of vari- ment nephropathy, gastrointestinal bleeding as a consequence ous distances per month.6 The Big Island of Hawai‘i is home of ischemic colitis, and ischemic hepatic injury. Interestingly to the world championship ironman triathlon, the ultimate test heat shock can lead to ; when the combination of high of endurance. Participants in these events are typically well temperature and reduced intestinal blood flow injures the conditioned and acclimatized, yet a determined athlete may intestinal wall, translocation of and other ignore warning signs.7 bacteria, toxins occurs through the portal vein and peritoneal Finally, Hawai‘i has a large military population. The military space.1,9 has classically been a leading source of literature on the preven- tion and management of heat illnesses. A soldier’s duties often Example Cases require engaging in vigorous activity while wearing heavy gear, Case 1 often under conditions which make adequate nutritional and A four-year-old child on vacation from Michigan spends the hydration status difficult to maintain. While training day on the beach. His parents remind him to drink water and are meant to simulate the stress of combat, not all soldiers are he finishes one water bottle over the course of the day. As the able to stand these conditions for prolonged periods of time.8 family packs up to leave, the boy’s parents notice he is less interactive than usual. He sits still and appears flushed. Thirty Clinical Description minutes later he is unresponsive and an ambulance is called. Heat illness occurs on a spectrum. The ICD 9 contains ten His vital signs are as follows: blood pressure, 80/50; heart rate, different diagnoses which categorize the physiologic mani- 130; respiratory rate, 24; oxygen saturation, 98% on room air; festations of excess heat stress. The umbrella term for these and a rectal temperature is measured at 105° F. Before the illnesses is heat injury (evidence of both hyperthermia and initial assessment is complete, the patient suffers a five minute end organ damage). We will discuss a few specific terms. The generalized tonic clonic which spontaneously abates. main distinction to note is the difference between intermediate His pupils are reactive but dilated. This patient has classic (non- and severe forms of heat illness. Intermediate illnesses have no exertional) heat stroke, in which the environment overwhelms neurologic impairment, while severe heat illness is a form of the patient’s ability to dissipate heat. distributive shock in which patients have altered or depressed mentation as a consequence. Case 2 Heat rash, characterized by pruritic papules due to occluded A thirty-year-old schoolteacher who lives in Kaneohe has sweat glands, and heat , painful muscle spasms attributed recently decided to get in shape. At the urging of a few of her to electrolyte abnormalities and dehydration, are both mild forms friends, she signs up for a fifteen mile trail run. She trains for of heat illness.1 Heat exhaustion presents with malaise, nausea only a week beforehand by running a few miles after work in and vomiting, headaches, and is classified as an intermediate the evenings. The race starts at 1000. It is a hot and humid day. severity form of heat illness. A patient’s vital signs may dem- Two miles from the finish line, she collapses. On assessment onstrate tachycardia and hypotension; however there is normal by the medical staff present, her rectal temperature is 104° F, mentation and no central nervous system involvement. Heat she is profusely sweating and disoriented when questioned. syncope, also called exercise associated collapse, falls within This patient has exertional heat stroke, in which intrinsic heat the intermediate range of illness as well. Both syndromes are production is the primary cause for hyperthermia. associated with slightly elevated core temperature.2 Heat shock is a multisystem illness, and is the most severe Case 3 form of heat illness. The hallmark features are core tempera- A 19-year-old military recruit is hospitalized after competing ture of 104° F or greater, encephalopathy, and additional evi- in the expert field medical badge. Following completion of the dence of end organ damage. Complications of heat shock are course, he collapses and is brought to the emergency room. numerous and usually attributable to ischemia and oxidative He recovers consciousness and on initial assessment there is damage. A systemic inflammatory response occurs as in other notable hypotension, temperature of 105° F, diffuse myalgias, forms of distributive shock. Clinical findings include tachy- elevated CK, acute renal failure with a Cr of 2.5, potassium of cardia, tachypnea, and hypotension, skin is warm and may be 6.0, electrocardiogram showed peaked T waves, and elevated hyperhidrotic or dry, pupils are often dilated from activation liver associated enzymes. He is immediately given fluids for his of the sympathetic nervous system, patients may have altered rhabdomyolysis, calcium chloride, albuterol, and with sensorium or even be comatose, and can occur. Heat dextrose for his hyperkalemia. A few hours after presentation, shock can be a cause of non-cardiogenic pulmonary edema he goes into hypoxic respiratory failure and is emergently in- and crackles may be auscultated. From a cardiac standpoint, tubated. The patient spends the next three days in the intensive

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 34 care unit requiring mechanical ventilation, vasopressor sup- and heart disease, should be obtained. port, and renal replacement therapy. This case highlights the If the cooling process initiated in the field has not lowered potential multi organ system involvement of heat shock and temperature to normal limits, it should be continued with ice associated disorders. water immersion or cutaneous application of ice packs in the hospital setting. Some studies show systemic cooling with a Treatment in Resource-Constrained central venous catheter is also effective; however the poten- Environments tial complications from the procedure outweigh any benefit Providing care for a patient with heat stroke involves three main over using conventional methods of cooling. Multiple studies concepts: stabilization of airway and circulation, rapid cool- have shown pharmacologic treatment, including non-steroidal ing, and finally transport to advanced care with monitoring for anti-inflammatories, acetaminophen, and dantrolene, have potential complications of heat illness. Sources agree that if the no outcome improvement, but may worsen complications. patient is otherwise stable, cooling should be addressed first and Therefore pharmacologic adjuncts to cooling are not generally transport second. Morbidity and mortality are directly related to recommended.10 the duration of core temperature elevation, and therefore rapid Laboratory studies should be obtained including a complete cooling is strongly stressed.3 blood count, electrolyte panel, creatine kinase level, urinaly- In an austere environment, materials to initiate cooling may sis, lactate, blood gas, hepatic function tests, and coagulation not be readily available. All equipment and excess clothing studies. An electrocardiogram and chest X-ray should also be should be immediately removed. The patient should be moved obtained. These studies are adequate to assess for the potential to a shaded area. Immersion in ice water is highly effective for complications of heat stroke discussed above. During assess- rapid cooling. The water should be stirred frequently during ment, continuous vital signs monitoring and telemetry should cooling to ensure continual contact with cool fluid. If ice water be initiated. is not available, any cool water source will suffice. A nearby Resuscitation with crystalloids should be aggressive and stream or pool of water can be used if no other options exist. titrated to improvement in vital signs and laboratory param- If ice is available but no tub, the patient can be placed in a tarp eters. Delirium and seizures are both treated with intravenous or sheet, covered with a large amount of ice, and then the tarp . Electrolyte abnormalities should be corrected or sheet can be wrapped around them. appropriately with removal or repletion. Many affected patients Alternatively, if immersion in water is not possible, applica- may need to be hospitalized for a period of observation and tion of cool wet cloths can be used, with frequent re-application monitoring for complications. Hypotension after fluid resus- as soon as the material warms. As much body surface area as citation, seizure, encephalopathy that is not rapidly resolving, possible should be covered when using this method. Spray- persistent oliguria, rhabdomyolysis, and evidence of gastroin- ing cool water over the patient is also an alternative method testinal bleeding, are all examples. Patients with signs of multi if available. Fanning may be helpful, however never allow a organ dysfunction or evidence of disseminated intravascular conscious patient to fan themselves as this will only generate coagulation are admitted to an intensive care setting.9 more heat via skeletal muscle contraction. 3 The importance of preventive measures should be stressed. Cooling via ice water immersion is estimated to occur at a Proper education regarding hydration, warning signs, and risk rate of approximately 1°C for every five minutes (1°F every factors is crucial in preventing heat illness. Acclimatization three minutes).3 If temperature monitoring is not possible, we by gradually increasing exertion in heat and maintenance of suggest cooling the patient for fifteen to twenty minutes, or cardiovascular fitness are also important. The physiologic until the patient begins to shiver. This allows for a reduction to adjustments that occur are expansion of the plasma volume, a safe temperature without risking over cooling. Other general earlier and increased sweating, lower salt concentration in sweat, interventions which should be performed in the field include and lower skin and core temperatures for a given amount of intravenous access if possible followed by fluid administration, exercise. Wet bulb globe temperature (WBGT) should be used or oral rehydration if the patient is able to tolerate oral intake. to predict environmental risk instead of ambient temperature alone. WBGT is a composite temperature used to estimate the Treatment in Non-Austere Environments effect of temperature, humidity, and wind speed on overall heat Research has shown mortality correlates with the degree of burden.7 Patients with risk factors for heat related illness should temperature elevation, time to initiation of cooling, and number be aware of their predilection. A variety of medications increase of organ systems involved. Management in the hospital setting risk, including diuretics, , and sympathomimet- should focus on modifying these factors. Continuous tempera- ics.1 ture monitoring should be initiated. External temperature is not Though an individual presenting with heat illness may appear reliable. Instead a bladder catheter with temperature probe, to have a straightforward etiology of their illness, a differential flexible rectal thermistor, or esophageal temperature monitor- diagnosis should still be considered. Clinical entities that could ing should be used.10 present with decreased consciousness, autonomic dysfunction, A detailed history regarding precipitation of the event, and hyperthermia include pontine or midbrain infarct, menin- medications, drugs of abuse, and medical history looking in gitis, drug induced , and parasitic infections such as particular for predisposing processes like sickle cell disease malaria.

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 35

Conclusion Author’s Affiliation: Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 Heat stroke continues to be a common and potentially lethal event. The method used for cooling is not crucial, instead the Correspondence to: speed of cooling and transport to advanced medical care is more Sarah Gordon MD; Tripler Army Medical Center, Honolulu, HI 96859; Email: [email protected] important prognostically. The recognized complications of heat stroke are numerous and in the worst case scenario it can result References in multiorgan failure. Thorough laboratory assessment as well 1. Knochel JP and Dallas MD. Environmental Heat Illness: An Eclectic Review. Arch Int Med. 1974;133(841-864). as electrocardiogram and chest X-ray should be performed upon 2. Morimoto RI. Cells in stress: transcriptional activation of heat shock genes. Science. arrival to a higher level of care to avoid missing complications. 1993;259(5100): 1409-1410. 3. Smith JE. Cooling methods used in the treatment of exertional heat illness. Br J Sports Med. Medical care is largely aimed at supportive therapy with cool- 2005;39:503–507. ing and intravenous crystalloids, with the goal of maintaining 4. KP, McCord C, Stevens D. Weather Data Management and archiving at the Maui High Performance Computing Center: Fire Conference 2000: The First National Congress on Fire normal vital signs and preventing end organ damage. Ecology, Prevention and Management, San Diego, 2000. 5. Stevens D. Hawaii Weather Climate Modeling Ohana. California/Nevada/Hawaii Meeting of Western Foresters. April, 2000. Maui, HI. Disclosures 6. Running races in Hawaii. http://runningroomhawaii.com/races/2013.html#top. Accessed 10 The author reported no conflicts of interest. Oct 2013. 7. Cipriani DJ, Swartz JD, Hodgson CM. Triathlon and the multisport athlete. J Orthop Sports Phys Ther. 1998;27(1):42-50. Disclaimer 8. Smalley B, Janke RM, Cole D. Exertional heat illness in Air basic military trainees. Military Medicine. 2003;168(4):298-303. The views expressed in this manuscript are those of the author 9. Abderrezak B, Knochel JP. Heat Stroke. N Engl J Med. 2002;346:1978-1988 and do not reflect the official policy or position of the Department 10. Glazer, JL. Management of heatstroke and heat exhaustion. American Family Physician. of the Army, Department of Defense, or the US Government. 2005;11(71) 2133-2136.

Ko‘olau Ridge Hike (Photo: Sarah Williams)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 36 Foreign Body Synovitis in the Pacific

Caleb Anderson MD; Rodger Stitt MD; and Jefferson Roberts MD

Abstract Foreign body synovitis in the Pacific region typically involves a penetrating Example Case Two: Retained injury to a joint. The introduced biomaterial produces an inflammatory reaction Foreign Body or innoculates the tissue with bacteria, creating an infection. Each year mil- A 33-year-old woman suffered a puncture from sea urchin spines lions of people visit the Hawaiian Islands to hike, surf, , and participate in the interphalangeal joint of her left hallux while surfing in in other outdoor activities, creating an array of interactions between people and nature. The two most commonly reported penetrating foreign body joint Sukuoka, Japan. The sea urchin spines were removed ten days injuries are sea urchin synovitis and synovitis due to implantation of organic later and she was started on broad spectrum antibiotics. Ra- material such as wood splinters or plant thorns. In this article we describe the diographs taken seven weeks post injury showed periarticular presentation, infectious profile, and treatment of these joint injuries. osteopenia, sub-articular cyst-like lucencies at the base of the distal phalanx, and subtle marginal erosion at the medial head Introduction of the proximal phalanx. An MRI done 8 weeks post injury Foreign body synovitis is a form of arthropathy, primarily showed a possible retained foreign body, although surgical monoarticular arthritis, resulting from an inflammatory re- exploration one week later yielded no foreign bodies and nega- action of the synovium due to a foreign object. The foreign tive cultures. At four months following the injury the patient fragments are characterized as either inorganic or organic. experienced worsening swelling and pain. Radiographs showed In this article, we will focus on foreign body synovitis from new extensive pari-articular erosion as well as worsening of the organic fragments. Typical materials that may cause organic subchondral cyst-like pathology of the distal phalanx. The patient foreign body synovitis include rose bush thorns, wood splin- was restarted on antimicrobial therapy including mycobacterial ters, starfish, coral, sea urchin spines, and shell fragments. A and fungal coverage. The patient experienced worsening pain common scenario is a young person who suffers a penetrating and range of motion and at nine months post injury was noted injury while working, gardening, hiking in the wilderness, or to have more extensive peri-articular erosions. At ten months swimming. The presence of foreign objects lodged in the joint post injury, a synovectomy, arthrodesis, and debridement of the can lead to an inflammatory reaction. Foreign objects can also interphalangeal joint were performed. No retained spine was seed the joint with bacterial or fungal elements producing a recovered, and histopathology was notable for granulomatous septic arthritis. It is important to rule out septic arthritis when synovitis with central fibrinoid as well as metaplastic evaluating possible foreign body synovitis. The synovitis may bone formation.2 be acute (hours to days after the injury), or chronic (months to years after the injury). This paper will describe the presentation, Discussion progression, diagnosis, and treatment of the two most common Foreign body synovitis secondary to implanted organic material causes of foreign body synovitis in the Pacific Region, namely is a common cause of monoarticular and tendon synovial tissue sea urchin synovitis and synovitis secondary to implantation inflammation and should always be on the list of differential of organic plant material. diagnoses in a patient presenting with joint swelling and ery- thema, even if a history of penetrating injury is not reported. If Example Case One: Retained Sea Urchin not removed and treated appropriately, acute synovitis, chronic Spines monoarticular synovitis, chronic bursitis, chronic tenosynovitis, A 55-year-old woman vacationing in Hawai‘i was or a soft-tissue foreign body cyst may result.3 Common causes when she was pushed against a rock by a large wave. Her hand of foreign body synovitis in the wilderness environment include landed on a sea urchin while bracing against the rock. She felt sea shell fragments, plant thorns, and sea urchin spines, with sudden pain and noted several purple puncture wounds on the synovitis secondary to sea urchin spike implantation and im- palmar surface at the base of her right ring finger. Her wound plantation of organic plant material being the most commonly was dressed at a local urgent care clinic but she noticed wors- reported in literature. ening stiffness and paresthesias in the ulnar distribution of her finger over the next few months. Ten weeks after the event an Sea Urchin Synovitis MRI demonstrated extensive flexor tenosynovitis as well as a Sea urchin injuries are a very common cause of foreign body possible foreign body. She was taken for surgical exploration synovitis in the Asia Pacific region. Sea urchins, also known which revealed multiple sea urchin spines embedded in the as wana in Hawaiian, are of the class Echinoidea of the echi- subcutaneous tissue, flexor digitorum superficialis tendon, and noderm phylum, with some 940 species. Wana are covered in flexor tendon sheath. The fragments were removed and extensive sharp spines attached via muscle and ball and socket joints. flexor tenosynovectomy was performed.1 Hawai‘i has at least three known species of sharp spined sea

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 37 urchins: Echinothrix calamaris, Echinothrix , and other inorganic foreign bodies such as and plastic, mostly Diadema paucispinum, all of which have either black or black due to inherent alkaloids (blackthorn) and oils and resins (many and white banded spines.4 The primary injury due to sea urchins types of wood).9 Progression to synovitis with wood splinters is spine penetration, usually of the hands, feet, or ankles.1 The and plant thorns is generally delayed, with one study finding a spines are brittle, and may break off in the wound.4 Sea urchin median interval of 68.5 days between injury and onset of joint spines are comprised of epithelial covered calcium carbonate pain/stiffness.10 which can cause an immediate reaction. The Most literature on plant thorn synovitis from the the Pacific wounds contain a purplish or black pigment, which can leave region involves the blackthorn shrub (Prunus spinous), date the impression that the spine is imbedded in the wound even if palm, or cactus. However, a case report of plant thorn synovitis it is not. When implanted in or near a joint, an acute inflamma- due to Zanthoxylum ailanthoides, an aromatic plant used as tory response, likely due to the epithelial covering, can occur, spice and found throughout East Asia, was reported in 2007. although it usually resolves within a matter of days. The initial This specific case was the first instance of plant thorn synovitis inflammatory response is generally followed by an asymptom- reported in Asia and was diagnosed by high-resolution ultra- atic period which can last days to years before progressing to sound. Synovectomy was the definitive treatment.11 synovitis. The articular pain in sea urchin synovitis is described Historically, plant thorn synovitis was considered an aseptic as being worse during periods of physical activity and at night, inflammatory reaction since most of the early literature failed to with physical examination showing periarticular swelling and grow a causative organism on culture, although joint aspiration varying degrees of joint effusion. Fever is seen more often in yielded a turbid fluid containing pus much like septic arthritis. synovitis due to sea urchin penetration than with wood splinters In the case of published literature on the blackthorn shrub, or or plant thorns. Also, regional lymphadenopathy, myalgias, and Prunus spinous, it was hypothesized that the joint inflammation synovitis of surrounding joints has been noted in sea urchin was secondary to alkaloids present in the thorn, although it was synovitis but generally not in synovitis due to vegetative mate- noted that antibiotics provided temporary symptomatic relief.3 rial. In two cases of divers stung multiple times with sea urchin It was not until literature published in 1977 that positive cultures spines, joint swelling at the old area of involvement was noted, were noted when three out of five patients were found to have raising the likelihood of a delayed hypersensitivity-like reaction.5 infectious aspirate growing Staphylococcus albus, gram negative Histologically, sea urchin synovitis is characterized by granu- rods, and alpha hemolytic strep.12 According to one literature loma formation in about 70% of cases, with histology showing review covering 1977 to 2008, of the 56 reported cases of plant sarcoid, necrobiotic, tuberculoid, and suppurative granulomas.6 thorn synovitis, 27% were found to have cultures positive for This chronic phase can progress to sea urchin spine arthritis if infectious organisms. Of these infectious cases, 73% were not appropriately treated, as in case two. It is unknown whether found to be due to Pantoea agglomerans (formerly referred calcium carbonate alone is responsible for this process, or if to as Enterobacter agglomerans), a facultative anaerobic gram another unknown antigen may play a role. Radiographic find- negative rod found commonly in soil and on vegetation. Other ings may mimic tuberculous or another atypical septic arthritis, implicated agents include Staphylococcus aureus, Enterobacter and it may progress to frank joint destruction relatively early in sp, and Nocardia asteroides.13 It is unclear whether this represents the disease course. Microorganisms are generally not isolated, a superinfection from a primarily sterile inflammatory process or with one study isolating no organisms out of five cases of hand whether these are the early culprits of the inflammatory reaction. synovitis by either culture or polymerase chain reaction (PCR), Patients with both septic and noninfectious plant thorn ar- and another study isolating in three thritis (ie, foreign body synovitis) often present afebrile with of eight specimens taken from seven patients.7,8 While there is a warm, swollen, and tender joint weeks to months after the a paucity of data on this subject, these reports, as well as the initial injury, and may not report a history of implantation. A outcome of case two, support that in sea urchin spine injuries delay of up to nine months in diagnosis has been reported.14 Joint conservative therapy with antimicrobial therapy and simple aspiration generally yields a turbid fluid with high leukocyte spine removal is ineffective and synovectomy with surgical count and polymorphonuclear leukocyte predominance. Both debridement is the preferred therapy.8 non-infectious plant thorn synovitis and septic arthritis can be quite dormant in presentation, especially considering that the Plant Thorn and Wood Splinter Synovitis majority of infections are due to Pantoea agglomerans, a quite Wood splinter and plant thorn implantation are very common indolent pathogen.13 This is why it is important to rule out septic in both children and adults, and while most superficial splinters arthritis before making the diagnosis of foreign body synovitis. can be extracted by the patients themselves, deeper splinters and those that break upon removal often require removal by a Treatment in Resource-Constrained trained health care provider. Complications from retained splin- Environments ters can include infection, inflammation, toxic reactions, and There are few reports in the medical literature on the initial granuloma formation, which can ultimately lead to synovitis if treatment of foreign body synovitis in the austere environment. imbedded in or near a joint space. Both plant thorns and wood In the case of sea urchin injury, the spine should be removed if it splinters are considered highly inflammatory as compared to is protruding. If it is not protruding, however, no attempt should

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 38 be made to remove the spine since the spine is very brittle and Conclusion can fragment. It has also been suggested to strike the affected Foreign body synovitis is common in the Pacific region and can area with a stone in an attempt to crush the spine and make it range from a chronic inflammatory state to a serious second- more easily resorbed.15 Home remedies have included using ary acute bacterial infection. It is important for the patient and vinegar and urine to attempt to dissolve the spine, although physician to suspect joint involvement after a penetrating injury there is no good evidence to support these claims. Application near the intra-articular joint space even if the injury appears of a salicylic-acid paste has also been used to attempt to dis- superficial. It is also important for the physician to realize that solved the spines. Immersion of the affected area in hot water each individual cause of foreign body synovitis has a different (110-115 F) has been found to provide pain relief initially, presentation, progression of disease, microbial profile, and risk of likely through inactivation of toxins, though this does nothing infection, and thus, different treatment. Patients presenting with to prevent long-term complications.16 Most interventions in the a vegetative foreign body have a much greater risk of secondary austere environment are anecdotal and have little if any support- infection due to the organic nature and porous structure of the ing evidence. Generally, all that can be done is to remove small body as compared to sea urchin spine, which is very seldom superficial splinters in the field before infection or inflammation found to be infectious.19 occurs, and to keep the injury site clean.17 A radiograph or other advanced imaging of the joint may aid in detection of a foreign body, although it is often negative Treatment in Non-Austere Environment and the disease process can progress even without concomitant In a non-austere environment, most patients with foreign body radiographic evidence of retained foreign body. If an inflam- synovitis present to the emergency department or their primary matory process is suspected, the joint should be aspirated and care physician with symptoms consistent with an acute, subacute, sent for cell count and culture. If clinical suspicion is high or chronic inflammatory monoarticular arthritis. The first step in enough, arthroscopic exploration and debridement should be a diagnostic evaluation is generally a plain radiograph, which considered. Untreated foreign body synovitis can cause serious may detect a foreign object depending on its density compared destruction of the joint and surrounding tissue if not treated to soft tissue. Imaging with a plain radiograph generally can early and appropriately. only detect radiodense material such as fish bone, sea urchin spines, or metal, and will usually miss wood or plant thorns, Disclosures with one study noting only 5% of wood splinters being seen The authors reported no conflicts of interest. on radiography.18 High resolution ultrasound, CT, and MRI imaging are quite efficacious at detecting wood splinters and Disclaimer plant thorns. Even with advanced imaging, small foreign objects The views expressed in this manuscript are those of the authors may remain unidentified.9 and do not reflect the official policy or position of the Department If a foreign body is found, the patient should be evaluated by of the Army, Department of Defense, or the US Government. an orthopedic surgeon for possible arthroscopic surgery with Authors’ Affiliation: debridement and irrigation. This is the recommended treatment Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 of choice since it is less invasive than synovectomy. Antibiot- ics may be indicated if there are signs of infection or if there Correspondence to: is an isolated organism from synovial culture. Joint infection Caleb Anderson MD; 1 Jarrett White Rd, Honolulu, HI 96859; Ph: (808) 433-4266; Email: [email protected] is much more likely with a retained wooden body than with a sea urchin spine. Reactive arthritis due to retained material References should be considered in cases with continued swelling and pain 1. Dahl W, Jebson P, Dean L. Sea urchin injuries to the hand: a case report and review of the literature. Iowa Orthop J. 2010;30:153-156. without positive cultures following initial arthroscopic surgery. 2. Schefflein J, Umans H, Ellenbogen D, Abad M. Sea urchin spine arthritis in the foot. Skeletal Arthrotomy is the preferred treatment for such refractory cases Radiology. 2012;41(10):1327-31. 3. Kelly JJ. Blackthorn inflammation. J Bone Joint Surg Br. 1966 Aug;48(3):474-7. because it will provide better visualization and more definitive 4. Thomas C, Scott S. All Stings Considered: and Medical Treatment of Hawaii’s Marine therapy.10 It has been suggested that sea urchin synovitis should Injuries. Honolulu, HI: University of Hawaii Press; 1997. 5. Reginato AJ, Ferreiro JL, O’Connor CR, Barbasan C, Arasa J, Bednar J. Clinical and pathologi- be treated initially with synovectomy given the high rate of cal studies of twenty-six patients with penetrating foreign body injury to the joints, bursae, and progression to arthritis and joint destruction. In one case series tendon sheaths. Arthritis Rheum. 1990;33:753-1762. 6. De La Torre C, Toribio J. Sea-urchin granuloma: histologic profile. A pathologic study of 50 of twelve patients with chronic sea urchin arthritis of the hand, biopsies. J Cutan Pathol. 2001 May;28(5):223-8. one patient required amputation of the affected finger and six 7. De la Torre C, Vega A, Carracedo A, Toribio J. Identification of Mycobacterium marinum in sea-urchin granulomas. Br J Dermatol. 2001 Jul;145(1):114-6. patients required surgical debridement, with a trend towards 8. Wada T, Soma T, Gaman K, Usui M, Yamashita T. Sea urchin spine arthritis of the hand. J better outcome with earlier synovectomy.8 Ensuring up to date Hand Surg Am. 2008 Mar;33(3):398-401. 9. Chan C, Salam GA. Splinter removal. Am Fam Physician. 2003;67(12):2557-62. vaccination status is very important in all cases of foreign 10. Nouh MR, Nasr AM, El-Shebeny MO. Wooden splinter-induced extremity injuries: Accuracy of body synovitis or penetrating trauma. MRI evaluation. The Egyptian Journal of Radiology and Nuclear Medicine. 2013 Sept;44(3):573-9.

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 39 11. Tung CH, Chen YH, Lan HH, Hsieh TY, Chen DY, Lan JL. Diagnosis of plant-thorn synovitis 15. Baden HP. Injuries from sea urchins. Clin Dermatology. 1987;5(3):112-7. by high-resolution ultrasonography: a case report and literature review. Clin Rheumatol. 2007 16. Böer A, Ochsendorf FR, Beier C, Kaufmann R. Effective removal of sea-urchin spines by May;26(5):849-51. erbium: YAG laser ablation. Br J Dermatol. 2001 Jul;145(1):169-70. 12. Sugarman M, Stobie DG, Quismorio FP, Terry R, Hanson V. Plant thorn synovitis. Arthritis 17. Carpenter CR, Schuur JD, Everett WW, Pines JM. Evidence-based diagnostics: adult septic Rheum. 1977 Jun;20(5):1125-8. arthritis. Acad Emerg Med. 2011 Aug;18(8):781-96. 13. Duerinckx J. Case report: subacute synovitis of the knee after a rose thorn injury: unusual 18. Levine MR, Gorman SM, Young CF, Courtney DM. Clinical characteristics and management clinical picture. Clin Orthop Relat Res. 2008;466:3138–42. of wound foreign bodies in the ED. Am J Emerg Med. 2008 Oct;26(8):918-22. 14. Zoltan JD. Cactus thorn synovitis. Arthroscopy. 1991;7:244–245. 19. O’Connell RL, Fageir MM, Addison A. Be aware of wood in the knee. BMJ CaseRep. 2011 Dec 13;2011.

Crown of thorns sea star (Acanthaster plancii) at night [Photo: Russell Gilbert MD]

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 40 Envenomation: Bringing the Pain to Hawai‘i and Pacific Islands

Joshua L. Fenderson MD

Abstract A 22-year-old gardener, with no risk factors for coronary ar- subspinipes is the only clinically significant centipede found in tery disease, developed ST elevation myocardial infarction after Hawai‘i. Envenomation typically leads to extreme localized pain, erythema, being bitten on his finger while working. His initial presentation induration, and tissue necrosis and possible lymphedema or lymphangitis. Mortality is uncommon and results from secondary infection or . was typical. He had severe pain and edema which subsided Management is supportive and includes wound care, pain control, and treat- over the next hour with application of cold and pressure to the ment with topical or oral antihistamines and anti-inflammatory medications. area. Approximately two hours after the bite, he began to have intense, retrosternal chest pain with nausea, diaphoresis, and Introduction radiation down his left arm. He presented to the emergency Centipede envenomations are frequent occurrences among department at fourteen hours after the bite with persistent hikers, campers and other visitors to Hawai‘i. It is not uncom- chest pain, but vital signs and examination were unremark- mon to find recipients of these bites in clinics or emergency able. His electrocardiograph showed ST segment elevations in rooms throughout the state.1 Bites from can cause the anterior leads and his cardiac enzymes were significantly extreme pain, edema, erythema and other localized symp- elevated. Echocardiography showed a hypokinetic anterior toms as well as anxiety and panic.2-4 Rarely, anaphylaxis wall and a left ventricular ejection fraction of 35%; coronary and death have occurred after a centipede bite. In a remote angiography was unremarkable. Three days after the bite, his setting where resources are limited, importance should be chest pain had resolved and his repeat electrocardiograph and placed on identification of the source of the bite and recogni- echocardiography were without abnormality.5 tion of common symptoms of centipede bites to distinguish A 44 year-old woman developed rhabdomyolysis and acute them from more serious and potentially fatal bites.4 kidney injury after a centipede bite to her right foot in her eastern home. Her immediate symptoms of localized Relevance To Hawai‘i And Asian Pacific pain, swelling, numbness and discoloration spread to involve Hawai‘i is home to three species of centipede Lithobius sp, her entire right leg over the following three days which drove Mecistocephalus maxillaries, and Scolopendra subspinipes. S. her to seek medical attention. She was referred to the University subspinipes is the only Hawaiian centipede with clinical signifi- of Arizona Health Sciences Center at five days after the bite cance and has a number of aliases, including Giant Centipede, due to worsening of her condition despite therapy. Jungle Centipede, Vietnamese Centipede, and Chinese Red She was found to be afebrile, but hypertensive and tachycardic Head. As is implied by these aliases, these centipedes are large with a marked non-erythematous swelling, warmth, and tender- and have a broad habitat that includes all of the Pacific islands. ness of her entire right lower extremity. She also had impaired Many residents and tourists engage in camping, hiking, motor function and abnormal sensation of her ankle and toes. and other outdoor activities that bring human and centipede She had 2+ blood on urine dipstick with two erythrocytes per into close proximity, setting the stage for bite occurrences.3 high power field on urine microscopy. Her serum creatinine was The actual incidence is difficult to determine since not all bite elevated to 11.4 mg/dl and hemodialysis was initiated within victims seek care, but a significant number of cases do get 24 hours of admission. She underwent three sessions of hemo- evaluated in emergency rooms. The Hawai‘i Department of dialysis with her renal function returning to near her baseline; Health’s most recent injury prevention plan reports that, of the however, she was found to have neurovascular compromise in unintentional injuries presenting to emergency departments with her right lower extremity due to compartment syndrome. Her a “natural or environmental” cause from 2007-2011, 11% were motor function and sensation improved with fasciotomy, but due to bites by centipedes.1 For perspective, 36% were due to her neurologic function was not fully recovered at the time the canine bites and 11% were due to stings from bees and wasps. report was written.6 The number of fatalities documented after centipede enven- Example Cases omation are few, and there is just one report that is well authen- Many human encounters with S. subspinipes and other centi- ticated. A publication from 1932 reports the case of a seven year pedes end in a startle at the expense of either or both parties. old female in the Phillipines who became severely ill and died Some may be unfortunate enough to experience the grasp of shortly after she was bitten on the head by a S. subspinipes cen- a centipede’s forcipules and the nagging pain and inflamma- tipede.7 Other fatalities have been reported but not substantiated. tion induced by envenomation. Very few, though, experience symptoms of such severity that their lives are at risk.

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 41 Discussion pain intensity and edema. The wound should be kept clean S. subspinipes is among the largest species of centipede measur- and should be covered to prevent contamination or secondary ing up to 20 cm in length. These have a brown or infection, and a tetanus immunization should be administered.4 redish head and dark green body with 21 total segments. From each segment extends one pair of yellow or yellow-orange legs. Treatment In Non-Austere Environments The legs attached to the head are modified into sharp claws, Many victims of centipede envenomation do not seek medi- called forcipules, which are hollow and connected to cal attention and most symptoms will resolve spontaneously. glands; and the legs attached to the final segment are long and Treatment of uncomplicated wounds does not greatly dif- prominent, extending behind the body. These centipedes are fer when limited resources are not a concern. Management easily distinguished from other centipedes in Hawai‘i by their should be supportive with wound care and control of pain and significant size since both Lithobius sp. and M. maxillaries inflammation being the mainstay of treatment. Initial heating reach just 5 cm in length. and later ice application is again suggested.3,4,8 Prophylactic S. subspinipes are fast and aggressive centipedes which strike antibiotics are generally unnecessary; however, if evidence of instinctively with little provocation. S. subspinipes is noctur- secondary infection is present, the wound should be cultured nally active, generally preying on other insects and arthropods; and a course of antibiotics which cover gram positive organ- however, these centipedes will feed on anything they can isms should be initiated. Benzodiazepines may be helpful in the overpower to include mice and small reptiles. During the day, centipede victim with symptoms of anxiety. 3 Cardiac ischemia they hide in moist and darkened areas, under logs, leaves, and and anaphylaxis are very rare complications and managing rocks. Shoes, clothing, bedding and sleeping bags are adequate these conditions with standard protocols takes priority over substitutions and common meeting places for human stings.2 treating localized symptoms. All patients presenting with S. subspinipes grasp victims with their forcipules and inject a centipede bites should be monitored in the emergency room venom comprised of a complex mix of chemicals, including for at least 4 hours for evidence of toxic shock.9 In addition, phospholipase A2, , and acidic proteins, from their bite victims should receive an immunization for tetanus.3,4,9 venom glands via hollow openings in the forcipules.4,8 In humans, this leads to immediate and often excruciating Conclusion burning pain followed by local edema and erythema. Lymph- Scolopendra subspinipes is the vector of all medically significant adenopathy and lymphangitis are also common. Tissue necrosis centipede envenomations in Hawai‘i. Though their bites can be may be seen at the forcipule puncture sites.3,4 The degree of very painful, serious morbidity is very uncommon. Treatment is symptoms varies from person to person and bite to bite. Pain primarily supportive in both the resource constrained and hospital and edema generally resolve spontaneously over a few days to settings, and therapy is directed at reducing pain, swelling, and one week, but can persist for up to three weeks.4 Cellulitis and anxiety. There is anecdotal evidence supporting the use of heat secondary infection occur, but are uncommon complications of soon after the bite has occurred with the goal of denaturing the S. subspinipes bites. Systemic reactions and death from centipede venomous proteins. Anaphalaxis, cardiac ischemia, or other seri- envenomation rarely occur, however, acute myocardial isch- ous complications are rare and should be managed according to emia in an adult male as well as death in a 7-year-old girl after existing treatment protocols. Victims of centipede bites should a bite to the head have been reported.3,8 Urticaria, anaphylaxis be monitored for four hours for development of symptoms of and rhabdomyolysis are also very rare complications which these complications, and all should receive a tetanus vaccination. have been attributed to envenomation by S. subspinipes. 3,4 Disclosure Treatment In Resource Constrained The author reported no conflicts of interest. Environment Data on treatment is limited and there is no standard or protocol Disclaimer that exists for management of these wounds. Treatment for cen- The views expressed in this manuscript are those of the author tipede bites is primarily supportive.3,4 In a resource constrained and do not reflect the official policy or position of the Department environment, it is helpful if the centipede is positively identi- of the Army, Department of Defense, or the US Government. fied because it can be difficult to distinguish a centipede bite from bites of other poisonous arthropods which require more Acknowledgements resource intensive management. Anesthetic, anti-inflammatory The author thanks the library staff at Tripler Army Medical Center for assisting and medications are suggested for control of pain with the literature review and the reviewers of this paper for their insightful comments and suggestions. and inflammation.4 Hot water or other mode of heat applica- tion soon after the bite occurs is thought to denature proteins Author’s Affiliation: in venom, reducing degree and duration of symptoms.3,4,8 After Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 the initial heat application, icing the bite area assists with re- 2 Correspondence to: duction in swelling and inflammation. For subjects with more Joshua L. Fenderson MD; Tripler Army Medical Center, Honolulu, HI 96859; severe symptoms, a short course of corticosteroids may decrease Email: [email protected]

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 42 References 5. Yildiz A. Acute myocardial infarction in a young man caused by centipede sting. Emergency 1. Injury Prevention Advisory Committee. 2012. Hawaii injury prevention plan 2012-2017, p. 3-4. Medicine Journal. 2006;23(4):e30-e30. doi:10.1136/emj.2005.030007. Hawaii State Department of Health. 6. Logan JL, Ogden DA. Rhabdomyolysis and acute renal failure following the bite of the giant 2. Yates JRI. Scolopendra subspinipes. Available at: http://www.extento.hawaii.edu/kbase/urban/ desert centipede Scolopendra heros. Western Journal of Medicine. 1985;142(4):549. Site/Centip.htm. Accessed October 13, 2013. 7. Lewis JGE. The Biology of Centipedes. Cambridge: Cambridge University Press; 1981. Avail- 3. Guerrero APS. Centipede bites in Hawai’i: a brief case report and review of the literature. Hawaii able at: http://ebooks.cambridge.org/ref/id/CBO9780511565649. Accessed March 2, 2014. Med J. 2007;66(5):125-127. 8. Auerbach PS, ed. Wilderness medicine. 6th ed. Philadelphia, PA: Elsevier/Mosby; 2012. 4. Bush SP, King BO, Norris RL, Stockwell SA. Centipede envenomation. Wilderness & environ- 9. Norris RL. “Centipede Envenomation”. eMedicine. 2008. Accessed October 17, 2013. mental medicine. 2001;12(2):93–99.

Ua mau ke ea o ka ‘aina i ka pono. The life of the land is preserved in righteousness.

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 43 Tropic Lightning: Myth or Menace?

John McCarthy MD

Abstract proposed explanations include increased urbanization, modern- Lightning is one of the leading causes of death related to environmental di- ization of rural infrastructure and farm equipment, and increased saster. Of all lightning fatalities documented between 2006 and 2012, leisure awareness and education regarding lightning safety.5-7 activities contributed the largest proportion of deaths, with water-associated, sports, and camping being the most common. Despite the prevalence of The most common lightning victim appears to be a male who these activities throughout the islands, Hawai‘i has had zero documented is engaging in a leisure activity, particularly a water-related lightning fatalities since weather data tracking was initiated in 1959. There is activity such as fishing or boating. Based on data gathered from a common misconception that lightning does not strike the ground in Hawai‘i. 238 lightning fatalities occurring from 2006 to 2012, males are This myth may contribute to a potentially dangerous false sense of security, more likely to be victims than females (82% vs 18%); leisure and recognition of warning signs and risk factor modification remain the most associated activities are the most common (64%); water-related important prevention strategies. Lightning damage occurs on a spectrum, (36%), sports (19%), and camping (10%) made up the top three from minor burns to multi-organ dysfunction. After injury, initial treatment should focus on “reverse triage” and immediate cardiopulmonary resuscitation most common activities; and of water-related lightning deaths, when indicated, followed by transfer to a healthcare facility. Definitive treat- the distribution included fishing (46%), boating (25%), beach 8 ment entails monitoring and management of potential sequelae, to include (20%), and swimming (9%). cardiovascular, neurologic, dermatologic, ophthalmologic, audiovestibular, Mechanisms of take five different forms. and psychiatric complications. A direct strike generally occurs when a person is in the open, and is the most likely to result in instantaneous death. Splash Background injury occurs when lightning strikes a nearby object and cur- Lightning physics is complex, but all lightning begins with a rent jumps or “splashes” via the path of least resistance (eg, thunderstorm. A thunderstorm develops when the sun heats nearby victim). Contact injury occurs when a victim is touching pockets of air that cause those pockets to rise in columns which an object that is hit by lightning. Ground current occurs when eventually form clouds. Within these clouds, layers of precipi- lightning strikes the ground near a victim and passes from the tation develop (ice, hail, rain), which based on their , strike point into the victim. A fifth mechanism involves passage stratify to different layers in the cloud. Rising warm air with of lightning from the victim upward. There are also instances of falling ice particles results in collisions between the different blunt injury due to the sheer concussive force of the associated particles. This creates charge, and eventually the top of the cloud thunder.1,3,9 becomes predominantly positive and the bottom of the cloud Lightning is unidirectional and produces a massive cur- negative.1 The earth is generally negatively charged, but when rent impulse of very short duration. The impulse can result storm clouds roll over, the negatively charged bottom of the in vaporization of skin moisture and blasting apart of clothes, cloud induces the earth to take on a positive charge.1,2 When rendering the victim naked. Unlike electrical injuries sustained the separation of charge becomes too much (a difference in from alternating current, the current of a only voltage between the cloud and the ground or object exceeds 2 remains internally for a very short time period, making deep million volts per minute), the result is lightning.2,3 tissue burns and myoglobinuric renal failure uncommon. Rather, Lightning strikes the earth approximately 8 million times that brief intense current may result in cardiac arrest ( a day or 100 times per second, making it one of the leading more than ); damage to the central, pe- causes of weather related death in the world.3 In the United ripheral, and/or autonomic nervous systems; superficial burns, States, according to the National Oceanic and Atmospheric ocular injuries (, corneal lesions, retinal detachment); Administration, there were 4002 fatalities from 1959 to 2012. ear injuries (tympanic membrane rupture, ossicle disruption, Climate, region, and season play a role in risk of lightning tinnitus); and psychological injury (fatigue, sleep disturbance, injury, as shown by the differences in incidence of lightning depression, memory problems).1,3 injury across the United States. Florida and Texas account for the most lightning fatalities (415 and 215 respectively), while Relevance to Hawai‘i and Asia Pacific Alaska and Hawai‘i (tied for 0) account for the least.4 Compared It is a common misconception that lightning does not strike to last century, despite increasing population density, there are the ground (or at all) in Hawai‘i. While it is true that lightning far fewer annual lightning fatalities. In the 1920s-1940s, the in Hawai‘i is far less common than on the mainland (the exact United States averaged around 400 lightning deaths per year. quantification remains elusive because the National Lightning In the last 50 years there was an average of 40 deaths annually, Detection Network does not include Hawai‘i), there are many and in the last three years, there was an average of 25 deaths examples of significant lightning events on the islands. In May annually. It is unclear why this decline is occurring, but some 2011, O‘ahu experienced a particularly impressive storm with

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 44 an estimated forty thousand cloud to ground lightning strikes Prevention: No location is absolutely safe from lightning. Large over a 30 hour period.10 In March 2012, lightning struck the structures and fully enclosed metal vehicles offer more protec- hull of a 36 foot catamaran in O‘ahu, and the boat sank to the tion than small open structures. Even while inside a structure, bottom of Keehi Lagoon Boat Harbor.11 A storm in Dec 2013 injury can occur with contact to conducting materials, as in the on the Big Island of Hawai‘i yielded an estimated ten to twenty case example above (the victim touched his faucet). Individuals thousand lightning strikes.12 No injuries were documented dur- should avoid touching metal during thunderstorms, to include ing any of these incidents. plumbing, telephones, and electronics. Areas to avoid would Lightning in the Hawaiian Islands is referenced in Hawaiian include open fields, tall structures (eg, flagpoles, trees), or being mythology. Pele is not only the goddess of fire, wind, and vol- near or in water (eg, oceans, beaches, pools). Efforts should canoes, but also lightning. In one story, Pele disguises herself focus on fleeing these areas, however if this is not possible and enters a store. She approaches a Chinese proprietor and and signs of imminent strike are present (as explained above), asks for a cup of coffee. When the proprietor refuses, Pele individuals should take the lightning position as last resort. unleashes lightning, causing the store to down and killing This position involves insulating oneself from the ground and the proprietor inside.13 minimizing points of contact. For instance, crouch with feet Aside from stories of Pele’s vengeance, Hawai‘i has had no together on a surface (eg, sleeping bag, backpack, official documented lightning fatalities since storm data tracking etc). Time spent in this position should be limited if access to was initiated in 1959. Hawai‘i is ranked last (tied with Alaska) more definitive safety is possible.5 in the least lightning fatalities per year (zero), and an estimated 0.1 injuries from lightning per 1 million people per year.4 Treatment: Most victims survive lightning injury if they receive The scarcity of lightning injuries may engender a false sense timely medical treatment. The most likely cause of death from of security. Hawai‘i is home to recreational activities (eg, water a lightning strike is cardiac arrest, and therefore if the victim is sports, camping, hiking, sporting events) at the highest risk for not breathing or without a pulse, advanced cardiac lightning injury. Therefore, individuals and providers should (ACLS) should be initiated as soon as possible with the fol- remain knowledgeable regarding recognition, prevention, and lowing considerations: (1) patients struck by lightning do not treatment strategies. carry electrical charge, and it is therefore safe to touch them, (2) caution must be exercised when running to save a lightning Example Case(s) victim, as the rescuer is often putting themselves at risk (there In July 2013, a 47-year-old man was inside his home in Maui is no explicit evidence that suggests lightning does not hit the during Hurricane Flossie. He was washing dishes, and when same place twice, and in fact, it often does), (3) ventilation must he reached to turn on the faucet, he saw a blue streak connect- often be supported, as due to suppression of the ing the faucet to his hand. The shock sent him to his knees, medullary respiratory center as well as thoracic muscle spasm but shortly after, he was able to walk to the living room to tell may persist despite return of spontaneous circulation , and (4) his wife what had happened. He reported hand numbness for even if appearing dead (fixed and dilated pupils), or the interval five minutes. His wife took his pulse, estimated at 180, and between injury and resuscitation has been prolonged, lightning subsequently called 911.14,15 patients have been known to respond to resuscitation. For this reason, if multiple victims are present, “reverse triage” should Treatment in Resource-Constrained be initiated, where those patients who are not breathing or are Environments without a pulse should actually be treated first.1,3,5,9 Recognition: The “30-30 Rule” is still often utilized, but may not be the current best practice. This rule suggests that if less Treatment in Non-Austere Environments than thirty seconds passes between seeing lightning and hearing In absence of cardiopulmonary arrest from the initial lightning corresponding thunder, then an individual should seek a safer strike, dying from lightning is a rare occurrence. Unfortunately, location.16 Although easy to remember, practice guidelines now of the 70%-90% of people who survive lightning injury, many express concern that this rule may instill a false sense of security. may still have permanent disability afterward.3 Getting struck A safer approach suggests that if lightning is seen or thunder by lightning can cause derangement in multiple organ systems, is heard, an individual is already at greater risk for lightning particularly related to cardiovascular, neurologic, dermatologic, injury and precautions should be initiated regardless of time eye, ear, and psychiatric manifestations. Recognition of high separation. Lightning is always associated with a thundercloud, risk is therefore important when determining need for closer but has been known to strike as much as 10 miles from the monitoring. These factors include suspected direct strike, any periphery of a storm. Therefore, lightning injury can still be loss of consciousness, focal neurologic complaints, chest pain, sustained after a storm has passed or even in sunny conditions, dyspnea, , cranial burns, leg burns or burns greater and individuals should wait at least 30 minutes from the most than 10% of total surface body area, or pregnancy.1,5 recent thunder clap or lightning sighting before resuming activi- Lightning causes massive simultaneous depolarization of ties. Signs of a more imminent strike include static electricity, the myocardium as well as possible muscle paralysis of chest nearby crackling, funny smells, or even “St. Elmo’s fire” (ie, a wall muscles and suppression of medullary respiratory center. blue haze around a person or object).5

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 45 Additional cardiopulmonary manifestations from lightning ation of other potential injuries (eg, corneal burns, intraocular strikes may include , elevated cardiac enzymes, hemorrhage, uveitis, orbital fractures). 1,3,5 cardiomyopathy, and ECG changes (ST elevation and QT Psychological and neurocognitive sequelae of lightning injury prolongation). As discussed above, this emphasizes the impor- are often delayed. Depression, changes in behavior, impaired tance of initial implementation of ACLS. Once resuscitation is memory, and difficulty with assimilation of new information achieved, high-risk patients should be admitted to the hospital have all been described in post-lightning strike syndrome. The for cardiac monitoring (at least 24 hours), screening ECG, and highest recovery rates are seen within the first year after injury, echocardiography.1,5 with mild improvement after three years. Antidepressants have Neurologic injury due to lightning strike varies widely in been found to be useful, but any dysfunction after three years severity. Most sustained neurologic injuries are transient, and in- is thought to be chronic, requiring long-term management. 1 clude loss of consciousness, headaches, paresthesias, confusion, seizures, and memory loss. Another phenomenon of neurologic Conclusion lightning injury is known as keraunoparalysis which is a transient In answering the question, “Tropic lightning: myth or menace?” paralysis of limbs thought secondary to massive overstimulation the answer is neither. Lightning in Hawai‘i, while less common of the autonomic nervous system. Subsequent vascular spasms compared to the mainland, does occur and has the potential to may be accompanied by pulselessness, cyanosis, and motor/ be just as dangerous. The lack of documented lightning fatalities sensory deficits. Close monitoring for compartment syndrome in Hawai‘i should not be construed to mean that lightning does should occur, but most instances of keraunoparalysis resolve not strike the ground, and the population should be educated spontaneously after several hours. Direct lightning strikes are regarding lightning safety. associated with intracranial hemorrhage, cerebral infarctions, and hypoxic encephalopathy (often secondary to cardiopulmo- Disclosure nary arrest). Delayed neurologic symptoms following lightning The author reported no conflicts of interest. strike (eg, progressive myelopathy) are also possible, which would warrant close follow up with a neurologist to establish Disclaimer a long term treatment plan.1,3,5 The views expressed in this abstract/manuscript are those of Whereas the American Burn Association recommends re- the author and do not reflect the official policy or position of ferral to a burn center for affected patients, generally, burns the Department of the Army, Department of Defense, or the sustained after lightning injury are more superficial, less severe, US Government. and quickly healing when compared to high-voltage electrical burns. In order to avoid contact burns after initial strike, metal Author’s Affiliation: Department of Medicine, Tripler Army Medical Center, Honolulu, HI 96859 objects (eg, jewelry) should be promptly removed. Internal burns resulting in underlying muscle damage, compartment Correspondence to: syndrome, and rhabdomyolysis are less common, however, John G. McCarthy MD; Tripler Army Medical Center, Honolulu, HI 96859; Email: [email protected] suspicion should remain, particularly in a hypotensive patient. Hypotensive patients require fluid resuscitation as well as References thorough evaluation for potential internal trauma caused by the 1. O’keefe gatewood M, Zane RD. Lightning injuries. Emerg Med Clin. North Am. 2004;22(2):369- 403. concussive force of the lightning injury. Full thickness burns 2. National Weather Service. Lightning safety: understanding lightning. Available at: http://www. are generally seen in areas of skin that had contact to metal lightningsafety.noaa.gov/science/science-overview.htm. Accessed January 18, 2014. 3. Ritenour AE, Morton MJ, Mcmanus JG, Barillo DJ, Cancio LC. Lightning injury: a review. Burns. objects or synthetic melted materials. Full thickness burns 2008;34(5):585-94. requiring grafting are generally uncommon in lightning injury, 4. National Weather Service. Lightning safety: statistics. Available at: http://www.lightningsafety. noaa.gov/statistics.htm. Accessed January 18, 2014. and patients with superficial burns that involve less than 20% 5. Davis C, Engeln A, Johnson E, et al. Wilderness medical society practice guidelines for the of total body surface area have been shown to heal relatively prevention and treatment of lightning injuries. Wilderness Environ Med. 2012;23(3):260-9. 1,3,5 6. Holle R, Lopez R, Navarro B. Deaths, injuries, and damages from lightning in the United States quickly. in the 1890s in comparison with the 1990s. Journal of Applied Meteorology. 2005;44:1563-72. Otologic and ophthalmologic findings after lightning injury 7. Rosen R. Almost no Americans die from lightning strikes anymore – why? January 14, 2014. The Atlantic. Available at: http://www.theatlantic.com/technology/archive/2014/01/almost-no- are also well documented. Blast overpressures from lightning americans-die-from-lightning-strikes-anymore-why/283046/. Accessed January 17, 2014. may result in tympanic membrane rupture and temporary 8. Jensenius JS. 2013: A detailed analysis of recent lightning deaths in the United States. NOAA lightning safety web site, www.lightningsafety.noaa.gov/resources/RecentLightningDeaths.pdf. deafness. Small perforations can be managed conservatively 9. Zafren K, Durrer B, Herry JP, Brugger H. Lightning injuries: prevention and on-site treatment in with bed rest and head elevation to prevent perilymph leakage. mountains and remote areas. Official guidelines of the International Commission for Mountain Emergency Medicine and the Medical Commission of the International Mountaineering and More severe injuries such as sensorineural deafness, vestibular Climbing Federation (ICAR and UIAA MEDCOM). Resuscitation. 2005;65(3):369-72. injury, or complex perforations will likely require specialized 10. Honolulu Star-Advertiser. 40,000 lightning strikes recorded during recent storm. May, 2011. Available at http://www.staradvertiser.com/news/breaking/121290058.html. Accessed January care. The most common eye injury from lightning is cataracts 04, 2014. which may occur soon after injury, or sometimes as late as four 11. Honolulu Star-Advertiser. Lightning sinks boat, damages two houses, knocks down rock wall. March 6, 2012. Available at http://www.staradvertiser.com/news/breaking/141713753.html. years after initial insult. Prompt referral to an ophthalmologist Accessed January 18, 2014. is always indicated in survivors of lighting injury, both for potential intervention (eg, steroids), as well as for closer evalu-

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 46 12. Herreria, Carla. Hawaii lightning storm video will trigger your first existential crisis of 2014. 15. Chao, Eileen. Maui News Now. July 2013. Available at: http://www.mauinews.com/page/content. January, 2014. Available at: http://www.huffingtonpost.com/2014/01/02/hawaii-lightning-storm- detail/id/574968/Woman—shocked—by-exaggeration.html. Accessed January 17, 2014. video_n_4534089.html. Accessed January 04, 2014. 16. Zimmermann C, Cooper MA, Holle RL. Lightning safety guidelines. Ann Emerg Med. 13. Nimmo HA. Pele, Volcano Goddess of Hawai’i, a History. (108). McFarland; 2011. 2002;39(6):660-4. 14. Lincoln, Mileka. Hawaii News Now. July 2013. Available at: http://www.hawaiinewsnow.com/ 17. Lederer W, Wiedermann FJ, Cerchiari E, Baubin MA. Electricity-associated injuries II: outdoor story/22973639/nws-flossies-intense-thunderstorms-rare-for-our-area.Accessed January 17, management of lightning-induced casualties. Resuscitation. 2000;43(2):89-93. 2014. 18. Cooper MA. A fifth mechanism of lightning injury. Acad Emerg Med. 2002;9(2):172-4.

Na Pali Trail Cliff Hike (Photo: William Harner MD)

HAWAI‘I JOURNAL OF MEDICINE & PUBLIC HEALTH, NOVEMBER 2014, VOL 73, NO 11, SUPPLEMENT 2 47 Hawai‘i Journal of Medicine & Public Health Public Health Manuscript Editors: Tonya Lowery St. John MPH Ranjani R. Starr MPH A Journal of Asia Pacific Medicine & Public Health Contributing Editors: ISSN 2165-8218 (Print), ISSN 2165-8242 (Online) Satoru Izutsu PhD Russell T. Stodd MD The Journal’s aim is to provide new scientific information in a scholarly manner, Carl-Wilhelm Vogel MD, PhD with a focus on the unique, multicultural, and environmental aspects Layout Editor & Production Manager: of the Hawaiian Islands and Pacific Rim region. Drake Chinen Subscription Manager: Published by University Clinical, Meagan Calogeras Education & Research Associates (UCERA) Editorial Board: Hawai‘i Journal of Medicine & Public Health Benjamin W. Berg MD, Patricia Lanoie Blanchette MD, 677 Ala Moana Blvd., Suite 1016B S. Kalani Brady MD, John Breinich MLS, Honolulu, Hawai‘i 96813 John J. Chen PhD, Donald Hayes MD, MPH, http://www.hjmph.org Satoru Izutsu PhD, Kawika Liu MD, Email: [email protected] Tonya Lowery St. John MPH, Jay Maddock PhD, The Hawai‘i Journal of Medicine & Public Health was formerly two separate Douglas Massey MD, Michael J. Meagher MD, journals: The Hawai‘i Medical Journal and the Hawai‘i Journal of Public Health. Alfred D. Morris MD, Myron E. Shirasu MD, The Hawai‘i Medical Journal was founded in 1941 by the Hawai‘i Medical Ranjani R. Starr MPH, Russell T. Stodd MD, Association (HMA), which was incorporated in 1856 under the Hawaiian Frank L. Tabrah MD, Carl-Wilhelm Vogel MD monarchy. In 2009 the journal was transferred by HMA to University Clinical, Statistical Consulting: Education & Research Associates (UCERA). The Hawai‘i Journal of Public Health was a collaborative effort between the Hawai‘i State Department of Health Biostatistics & Data Management Core, and the Office of Public Health Studies at the John A. Burns School of Medicine John A. Burns School of Medicine, established in 2008. University of Hawai‘i (http://biostat.jabsom.hawaii.edu)

Editors: Advertising Representative S. Kalani Brady MD Roth Communications Michael J. Meagher MD 2040 Alewa Drive, Honolulu, HI 96817 Editor Emeritus: Phone (808) 595-4124 Norman Goldstein MD The Hawai‘i Journal of Medicine & Public Health (ISSN 2165-8218) is a monthly peer-reviewed journal published by Associate Editors: University Clinical, Education & Research Associates (UCERA). The Journal cannot be held responsible for opinions Donald Hayes MD, MPH expressed in papers, discussion, communications, or advertisements. The right is reserved to reject material submitted for editorial or advertising columns. Print subscriptions are available for an annual fee of $220; single copy $20 includes Kawika Liu MD postage; contact the Hawai‘i Journal of Medicine & Public Health for foreign subscriptions. Full text articles available on Jay Maddock PhD PubMed Central. ©Copyright 2014 by University Clinical, Education & Research Associates (UCERA). Copy Editor: Alfred D. Morris MD

Na Pali Cliffs from Kalalau (Photo: William Harner MD)